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Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I
Open accessAbstract
Oxidative damage from elevated production of reactive oxygen species (ROS) contributes to ischemia-reperfusion injury in myocardial infarction and stroke. The mechanism by which the increase in ROS occurs is not known, and it is unclear how this increase can be prevented. A wide variety of nitric oxide donors and S-nitrosating agents protect the ischemic myocardium from infarction, but the responsible mechanisms are unclear. Here we used a mitochondria-selective S-nitrosating agent, MitoSNO, to determine how mitochondrial S-nitrosation at the reperfusion phase of myocardial infarction is cardioprotective in vivo in mice. We found that protection is due to the S-nitrosation of mitochondrial complex I, which is the entry point for electrons from NADH into the respiratory chain. Reversible S-nitrosation of complex I slows the reactivation of mitochondria during the crucial first minutes of the reperfusion of ischemic tissue, thereby decreasing ROS production, oxidative damage and tissue necrosis. Inhibition of complex I is afforded by the selective S-nitrosation of Cys39 on the ND3 subunit, which becomes susceptible to modification only after ischemia. Our results identify rapid complex I reactivation as a central pathological feature of ischemia-reperfusion injury and show that preventing this reactivation by modification of a cysteine switch is a robust cardioprotective mechanism and hence a rational therapeutic strategy.
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“Conversely, S-nitrosation of the other three cysteines was unaffected by changes in complex I activity (Fig. 2d and Supplementary Figs. 8–10).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO reproducibly S-nitrosated three subunits: the 75 kDa, B8 and ND3 subunits (Fig. 2b,c, Supplementary Fig. 7b and Supplementary Table 2).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Notably, MitoSNO treatment did not inhibit complex I in the normoxic myocardium in vivo (Fig. 1g)”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO administered at reperfusion significantly decreased infarct size (Fig. 1b and Supplementary Fig. 2).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“we identified four cysteines that were S-nitrosated by MitoSNO: two on the 75 kDa subunit and one each on the ND3 and B8 subunits (Fig. 2c,d and Supplementary Table 3).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Using this method, we found that only respiratory complex I and the FoF1-ATP synthase were detectably S-nitrosated within mitochondria in vivo (Fig. 1f, Supplementary Fig. 6a and Supplementary Table 1).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In the MitoSNO-treated mice, complex I activity returned to its initial levels after 30 min”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Although S-nitrosation did not affect FoF1-ATP synthase activity (Supplementary Fig. 6b)”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO did not alter hemodynamics (Supplementary Fig. 4).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“S-nitrosation of ND3 Cys39 was negligible under conditions of high activity but increased markedly under conditions of low activity (Fig. 2d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Neither SNAP nor the MitoSNO-targeting moiety (MitoNAP)11 had this effect (Fig. 1b).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In contrast, in the absence of MitoSNO treatment in vivo, complex I was not affected after 5 min of reperfusion, but its activity then decreased by ~50% during 30 min of reperfusion and could not be restored ex vivo by reductants”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Within the intact, ischemic heart perfused ex vivo in a Langendorff system, there was substantial (~40%) S-nitrosation of ND3 by MitoSNO that was not present in normoxic hearts; in contrast, the amount of S-nitrosation of the 75 kDa subunit cysteines was similar under normoxia and ischemia (Fig. 3a, Supplementary Table 4 and Supplementary Fig. 11).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO administered at reperfusion blocked this rise in the amount of hydrogen peroxide, whereas administration of SNAP did not (Fig. 1c).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“This led to the selective S-nitrosation of mitochondrial proteins in the reperfused heart (Fig. 1a), as visualized by labeling with a red fluorescent probe15–17. In contrast, equal doses of the untargeted precursor S-nitrosating compound S-nitroso-N-acetylpenicillamine (SNAP) S-nitrosated only nonmitochondrial myocardial and plasma proteins (Fig. 1a).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Intravenous injection of MitoSNO into mice also resulted in S-nitrosation of the ND3 cysteine in vivo during reperfusion of the ischemic heart, whereas MitoSNO injection did not have this effect in normoxic hearts (Fig. 3b).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Complex I activity was lower in heart mitochondria from MitoSNO-treated mice compared to untreated mice, and this decreased activity was normalized by selective S-nitrosothiol reduction using copper and ascorbate15–17 (Fig. 1g).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Moreover, ND3 Cys39 was extensively S-nitrosated (>50%) by MitoSNO in isolated rat heart mitochondria during anoxia but was negligibly modified under normoxic conditions (Fig. 2e,f).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO was protective only during reperfusion: injection 10 min after reperfusion was ineffective (Supplementary Fig. 3).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Using MitoB we found that the amount of mitochondrial hydrogen peroxide remained low during ischemia and increased only after reperfusion in vivo (Fig. 1c).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“The rise in the amount of mitochondrial hydrogen peroxide was associated with increased protein carbonylation (Fig. 1d), a marker of oxidative damage, as well as necrotic (Fig. 1b) and apoptotic (Fig. 1e) cell death, and these effects were all prevented by MitoSNO.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO protected control cardiomyocytes treated with a scrambled RNAi construct from ischemia-reperfusion injury, but decreasing complex I activity by NDUFAF1-targeted RNAi completely abolished MitoSNO protection (Fig. 4a).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Copper and ascorbate treatment restored complex I activity, indicating that the inhibition of activity was due to S-nitrosation of ND3 Cys39 (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Exposure of isolated bovine heart mitochondrial membranes to MitoSNO under conditions in which complex I is in a high activity state led to S-nitrosation of the 75 kDa and B8 subunit cysteines but not of the ND3 subunit, and this exposure did not affect complex I activity (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“We selectively knocked down expression of the complex I assembly factor NDUFAF1 (ref. 36) by RNAi, which decreased protein amounts by 80% (Supplementary Fig. 16a–c) and lowered complex I activity (Supplementary Fig. 16d) while leaving the amount of complex II unaffected (Supplementary Fig. 16a,e).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [36] Mimaki, M. et al. Understanding mitochondrial complex I assembly in health and disease. Biochim. Biophys. Acta 1817, 851–862 (2012). source
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“Our model shows that Cys39 is located at the hinge region of complex I facing the mitochondrial matrix. Furthermore, Cys39 is adjacent to the half-channel element of one of the four proposed proton translocation pathways of complex I and is close to the ubiquinone binding pocket, where ubiquinone receives electrons from the N2 iron-sulfur center (Fig. 3g)34.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [34] Baradaran, R., Berrisford, J.M., Minhas, G.S. & Sazanov, L.A. Crystal structure of the entire respiratory complex I. Nature 494, 443–448 (2013). source
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- Rests on an assumption: The prokaryotic complex I structures used for modeling are sufficiently homologous to mammalian complex I to locate ND3 Cys39 accurately.
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In the paper
“Nitrite infusion during prolonged ischemia resulted in substantial S-nitrosation of this cysteine, which was negligibly modified by nitrite under normoxic conditions (Fig. 4b,c and Supplementary Table 5).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In contrast, incubation with MitoSNO under conditions in which complex I is in a low activity state led to S-nitrosation of ND3 Cys39, as well as of the other three cysteines, and inhibited complex I activity (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“Together these data indicate that cardioprotection by MitoSNO acts through mitochondrial S-nitrosation, which inhibits mitochondrial hydrogen peroxide production at reperfusion.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“As complex I was the only S-nitrosation target identified in our proteomic analysis whose activity was affected by this modification, we consider it to constitute a probable node for cardioprotection.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO has been reported to be protective in mice with cardiomyocyte deficiency of protein kinase G18, indicating that the cardio-protection conferred by MitoSNO is not due to nonmitochondrial pathways that operate through cyclic GMP–protein kinase G signaling3,6”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [18] Methner, C., Lukowski, R., Hofman, F., Murphy, M.P. & Krieg, T. Protection through postconditioning or a mitochondria-targeted S-nitrosothiol is unaffected by cardiomyocyte-selective ablation of protein kinase G. Basic Res. Cardiol. 108, 337 (2013). source
- Not checked yetcites [3] Lundberg, J.O., Weitzberg, E. & Gladwin, M.T. The nitrate-nitrite–nitric oxide pathway in physiology and therapeutics. Nat. Rev. Drug Discov. 7, 156–167 (2008). source
- Not checked yetcites [6] Costa, A.D. et al. Protein kinase G transmits the cardioprotective signal from cytosol to mitochondria. Circ. Res. 97, 329–336 (2005). source
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In the paper
“previous work has shown that complex I is inhibited by various nitric oxide donors in vitro and that this inhibition is associated with S-nitrosation2,10,11,21–24.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [2] Shiva, S. et al. Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer. J. Exp. Med. 204, 2089–2102 (2007). source
- Not checked yetcites [10] Sun, J., Morgan, M., Shen, R.F., Steenbergen, C. & Murphy, E. Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transport. Circ. Res. 101, 1155–1163 (2007). source
- Not checked yetcites [11] Prime, T.A. et al. A mitochondria-targeted S-nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury. Proc. Natl. Acad. Sci. USA 106, 10764–10769 (2009). source
- Not checked yetcites [21] Clementi, E., Brown, G.C., Feelisch, M. & Moncada, S. Persistent inhibition of cell respiration by nitric oxide: crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione. Proc. Natl. Acad. Sci. USA 95, 7631–7636 (1998). source
- Not checked yetcites [22] Burwell, L.S., Nadtochiy, S.M., Tompkins, A.J., Young, S. & Brookes, P.S. Direct evidence for S-nitrosation of mitochondrial complex I. Biochem. J. 394, 627–634 (2006). source
- Not checked yetcites [23] Dahm, C.C., Moore, K. & Murphy, M.P. Persistent S-nitrosation of complex I and other mitochondrial membrane proteins by S-nitrosothiols but not nitric oxide or peroxynitrite. J. Biol. Chem. 281, 10056–10065 (2006). source
- Not checked yetcites [24] Galkin, A. & Moncada, S. S-nitrosation of mitochondrial complex I depends on its structural conformation. J. Biol. Chem. 282, 37448–37453 (2007). source
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In the paper
“These data suggest that complex I ND3 Cys39 is the crucial functional S-nitrosation target and that other interactions of MitoSNO with mitochondria do not contribute to protection.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“This mechanism probably contributes to cardioprotection by untargeted nitric oxide donors and alterations to nitric oxide metabolism in general, although nonmitochondrial pathways may also contribute.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“We assessed infarct size after 120 min of reperfusion using triphenyltetrazolium chloride staining and expressed it as a percentage of the risk zone as described recently40.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
What the sources say
- Not checked yetcites [40] Nadtochiy, S.M., Redman, E., Rahman, I. & Brookes, P.S. Lysine deacetylation in ischaemic preconditioning: the role of SIRT1. Cardiovasc. Res. 89, 643–649 (2011). source
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In the paper
“We used an open-chest, in situ mouse (C57BL/6) heart model as recently described41.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
What the sources say
- Not checked yetcites [41] Schmidt, K. et al. Cardioprotective effects of mineralocorticoid receptor antagonists at reperfusion. Eur. Heart J. 31, 1655–1662 (2010). source
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In the paper
“The nitrite (NO2−) anion protects from ischemia-reperfusion injury in vivo1–3,37 and is thought to act as an S-nitrosating agent in the ischemic myocardium2.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [1] Duranski, M.R. et al. Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver. J. Clin. Invest. 115, 1232–1240 (2005). source
- Not checked yetcites [2] Shiva, S. et al. Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer. J. Exp. Med. 204, 2089–2102 (2007). source
- Not checked yetcites [3] Lundberg, J.O., Weitzberg, E. & Gladwin, M.T. The nitrate-nitrite–nitric oxide pathway in physiology and therapeutics. Nat. Rev. Drug Discov. 7, 156–167 (2008). source
- Not checked yetcites [37] Shiva, S. & Gladwin, M.T. Nitrite mediates cytoprotection after ischemia/reperfusion by modulating mitochondrial function. Basic Res. Cardiol. 104, 113–119 (2009). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“As the S-nitrosation of the ND3 subunit only occurs after anaerobic incubation, these findings suggest that MitoSNO decreases ROS production by S-nitrosating the ND3 subunit.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“To assess differences in protein fluorescence using two-dimensional DIGE, we used an experimental design that included biological variance analysis (BVA)12. In each DIGE experiment, we used four biological replicates, where a biological replicate is an independently prepared heart tissue subjected to the CyDye sample preparations described above.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > SNO-DIGE experimental design
What the sources say
- Not checked yetcites [12] Chouchani, E.T. et al. Identification of S-nitrosated mitochondrial proteins by S-nitrosothiol difference in gel electrophoresis (SNO-DIGE): implications for the regulation of mitochondrial function by reversible S-nitrosation. Biochem. J. 430, 49–59 (2010). source
plainn = 4- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one. The quote only partly states this claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We scanned all gels at 100- to 200-μm pixel size, and the photomultiplier tube was set to ensure a maximum pixel intensity within the linear acquisition range for the region of the gel being analyzed (most commonly the sub–20 kDa region of gels containing the complex I ND3 subunit) and thereby ensuring that fluorescent signal intensities were in the linear range.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Gel imaging and analysis
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“All samples were shielded from light throughout the experiment to preserve S-nitrosothiols.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Mitochondrial preparations and incubations
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Reperfusion of the ischemic tissue rapidly reactivates complex I and generates hydrogen peroxide, which causes oxidative damage that leads to the cell death underlying ischemia-reperfusion injury.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“All animal experiments described here were carried out in accordance with the UK Home Office Guide on the Operation of Animal (Scientific Procedures) Act of 1986 and the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication 85–23, revised 1996). All procedures were approved under the Project License number PPL 80/2393.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“As the ND3 subunit is encoded by mitochondrial DNA, its cysteine cannot be replaced genetically, and there are no known natural mutations or polymorphisms in the gene encoding this subunit (MT-ND3)31.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [31] Bridges, H.R., Birrell, J.A. & Hirst, J. The mitochondrial-encoded subunits of respiratory complex I (NADH:ubiquinone oxidoreductase): identifying residues important in mechanism and disease. Biochem. Soc. Trans. 39, 799–806 (2011). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Together these data suggest that ischemia exposes ND3 Cys39 for S-nitrosation and that this modification specifically mediates the reversible inhibition of complex I in vivo.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This result indicates that S-nitrosation of ND3 Cys39 does not disrupt complex I function by affecting the interaction of NADH with the flavin mononucleotide site and that the S-nitrosation of other residues in complex I does not affect its activity.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“We incubated mitochondria or mitochondrial membranes from both the in vitro and in vivo treatment groups in 100 mM NEM to quench unreacted thiols.”
- Also stated in: § Differential labeling of respiratory complex I S-nitrosothiols · plain
“Mitochondria from mice treated in vivo with an S-nitrosating agent were isolated as described above in buffer supplemented with 100 mM NEM before differential labeling.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Differential labeling of respiratory complex I S-nitrosothiols
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Differential labeling of respiratory complex I S-nitrosothiols · plain
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“When protein S-nitrosothiols were to be assessed in mitochondria isolated from hearts that had been subjected to in vivo treatments, 100 mM NEM was included in the isolation buffers.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Mitochondrial preparations and incubations
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When S-nitrosating species are present during reperfusion, the exposed ND3 cysteine becomes S-nitrosated, locking complex I in a low activity state and decreasing ROS production during the reperfusion phase.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Pelleted samples were washed three times in Chelex 100–treated PBS before resuspension in 100 μl of the same buffer containing 1 mM ascorbate and 10 μM CuSO4”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Differential labeling of respiratory complex I S-nitrosothiols
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Error bars represent the s.e.m. from at least three replicates unless otherwise stated.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Statistical analyses
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“For analysis, we spiked the tissues with deuterated internal standards, extracted the MitoB and its product MitoP from the reaction with hydrogen peroxide and determined the amounts of MitoB and MitoP present in the tissue by liquid chromatography and tandem mass spectrometry as described previously20.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of mitochondrial hydrogen peroxide flux in vivo
What the sources say
- Not checked yetcites [20] Cochemé, H.M. et al. Measurement of H2O2 within living Drosophila during aging using a ratiometric mass spectrometry probe targeted to the mitochondrial matrix. Cell Metab. 13, 340–350 (2011). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“MitoSNO stability was assessed before use from its absorbance at 340 nm.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Chemical syntheses
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“NO2− and control saline infusions began 15 min before ischemia and continued throughout the ischemic phase so that a constant final concentration of NO2− was maintained in the heart.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“We measured mitochondrial hydrogen peroxide in vivo using the MitoB mass spectro-metric probe as described previously20.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of mitochondrial hydrogen peroxide flux in vivo
What the sources say
- Not checked yetcites [20] Cochemé, H.M. et al. Measurement of H2O2 within living Drosophila during aging using a ratiometric mass spectrometry probe targeted to the mitochondrial matrix. Cell Metab. 13, 340–350 (2011). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“We treated mouse hearts with nitrite using previously established protocols known to elicit cardioprotection38.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
What the sources say
- Not checked yetcites [38] Webb, A. et al. Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage. Proc. Natl. Acad. Sci. USA 101, 13683–13688 (2004). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“In parallel, we determined the citrate synthase activity of each sample46. We then normalized the complex I rate to the citrate synthase rate and expressed it as a percentage of the appropriate control.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of complex I activity
What the sources say
- Not checked yetcites [46] Srere, P.A. Citrate synthase. Methods Enzymol. 13, 3–10 (1969). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“When administering NO2− or saline solutions to ischemic hearts, we deoxygenated the solutions during preparation by bubbling with 95% N2 and 5% CO2.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We protected cells from light during hypoxia (2 h) and reperfusion (1.5 h) and measured cell death using a lactate dehydrogenase (LDH) release assay (Cytotoxicity Detection, Roche Applied Science) according to the manufacturer's instructions.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vitro ischemia reperfusion injury to cells
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Before this study, the existence and physiological importance of S-nitrosation of complex I in vivo had not been demonstrated.
“However, to our knowledge, the existence and physiological importance of S-nitrosation of complex I in vivo has not previously been demonstrated.”
The paper relies on this without support.
The conservation of ND3 Cys39 across metazoans implies that this residue has a physiological role.
“Cys39 in ND3 is conserved throughout metazoans, consistent with a physiological role for this residue.”
The paper relies on this without support.
The prokaryotic complex I structures used for modeling are sufficiently homologous to mammalian complex I to locate ND3 Cys39 accurately.
“We modeled the location of ND3 Cys39 using structures of prokaryotic complex I (refs. 32–34). This modeling led to an orthologous mammalian core structure containing ND3 Cys39”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Mechanistically, this protection is dependent on MitoSNO transnitrosating a critical cysteine in the active site of complex I.”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“This S-nitrosation of Cys39 in the ND3 subunit of complex I inhibits its catalytic activity and, hence, attenuates reverse electron transport and ROS production (170).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“For example, MitoSNO (FIGURE 14), a mitochondrially targeted S-nitrosothiol, was shown in rodent models to significantly attenuate infarct size after MI (170).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“Murphy and coworkers used a mitochondria-selective S-nitrosating agent to demonstrate that nitrosation of Complex I serves a protective role during ischemia/reperfusion by reducing oxidative damage and tissue necrosis [212, 213].”
From Signaling and stress: The redox landscape in NOS2 biology (2015) · cites this paper as [213]
Citations
Cites
Perkins, D. N., Pappin, D., Creasy, D. M., & Cottrell, J. S. (1999) · Electrophoresis · doi:10.1002/(sici)1522-2683(19991201)20:18 · Cited by 8,264
Yellon, D. M., & Hausenloy, D. J. (2007) · New England Journal of Medicine · doi:10.1056/nejmra071667 · Cited by 3,797
The nitrate-nitrite-nitric oxide pathway in physiology and therapeutics
Lundberg, J. O., Weitzberg, E., & Gladwin, M. T. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2466 · Cited by 2,739
Srere, P. A. (1969) · Methods in Enzymology · doi:10.1016/0076-6879(69)13005-0 · Cited by 2,005
Wittig, I., Braun, H., & Schägger, H. (2006) · Nature Protocols · doi:10.1038/nprot.2006.62 · Cited by 1,741
Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury
Murphy, E., & Steenbergen, C. (2008) · Physiological Reviews · doi:10.1152/physrev.00024.2007 · Cited by 1,504
Clementi, E., Brown, G. C., Feelisch, M., & Moncada, S. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.13.7631 · Cited by 863
Crystal structure of the entire respiratory complex I
Baradaran, R., Berrisford, J. M., Minhas, G. S., & Sazanov, L. A. (2013) · Nature · doi:10.1038/nature11871 · Cited by 797
Structure of the Hydrophilic Domain of Respiratory Complex I from Thermus thermophilus
Sazanov, L. A., & Hinchliffe, P. (2006) · Science · doi:10.1126/science.1123809 · Cited by 763
Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver
Duranski, M. R., Greer, J. J. M., Dejam, A., Jaganmohan, S., Hogg, N., Langston, W., Patel, R. P., Yet, S.-F., Wang, X., Kevil, C. G., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci22493 · Cited by 674
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“NO has been implicated in modulating FA uptake and utilization in the mammalian myocardium from normal heart [4,14,15,23,24] Furthermore, nNOS may affect myocardial function via regulating mitochondrial proteins since nNOS-derived NO has been shown to inhibit mitochondrial respiration chain, including complex I, III a…”
BackgroundLau, G. Y., & Richards, J. G. (2018) · Journal of Experimental Biology · doi:10.1242/jeb.189407 · Cited by 6
“Interspecific variation in how brain mitochondria recover from in vitro anoxia exposure Injury is sustained from ischemia–reperfusion as a result of the surge of ROS generated in normoxic recovery following a period of O2 deprivation (Chouchani et al., 2013).”
BackgroundYang, H., Wang, L., Xie, Z., Shao, S., Wu, Y., Xu, W., Gu, B., & Wang, B. (2023) · Journal of Chromatography A · doi:10.1016/j.chroma.2023.464162 · Cited by 6
Yang, Z., Jiang, X., & Gao, J. (2024) · International Journal of Pharmaceutics · doi:10.1016/j.ijpharm.2024.125069 · Cited by 5
Nakamura, T., Sharma, A., & Lipton, S. A. (2025) · Neurotherapeutics · doi:10.1016/j.neurot.2025.e00708 · Cited by 5
“S-Nitrosylation of Cys39 blocks this reactivation process to transiently lock complex I in the D-state and prevents toxic ROS production, providing cardioprotection against acute ischemia/reperfusion [107].”
Alpha-ketoglutarate dehydrogenase: more than just a TCA cycle enzyme
Mailloux, R. J. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.02.050 · Cited by 5
Charidemou, E., Andreou, E. P., & Papaneophytou, C. P. (2026) · Biomolecules · doi:10.3390/biom16060867 · Cited by 7
“Limiting succinate accumulation (e.g., SDH inhibition) or preventing RET at reperfusion (e.g., reversible Complex I inhibitors) reduces infarct size in preclinical models [142,143].”
Plant supercomplex I + III2 structure and function: implications for the growing field
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Brucella induced upregulation of NO promote macrophages glycolysis through the NF-κB/G6PD pathway
Cao, S., Guo, J., Zhu, D., Sun, Z., Liu, L., Zhang, Y., Maratbek, S., Wang, Z., Zhang, J., Li, W., et al. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.113038 · Cited by 6
Galambo, D., & Bergdahl, A. (2022) · Current Research in Physiology · doi:10.1016/j.crphys.2022.100097 · Cited by 5
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“RET-ROS has been implicated in redox signaling during inflammation and mitochondrial uncoupling in adipose tissue [15 – 17], aging in flies [18], or ischemia – reperfusion of the heart [19,20].”
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“Suggestively, S-nitrosation has been implicated in the regulation of a number of proteins previously linked to cell survival and proliferation, as well as NO production and mitochondrial function, including NF-κB,(65,69) caspase-3,(65) p53,(65) Ras,(65,70) several components of the MAP kinase pathway,(65) all three NO…”
BackgroundArriagada, O., Treuer, A. V., & González, D. R. (2018) · InTech eBooks · doi:10.5772/intechopen.77003 · Cited by 4
The Promise of a Golden Era for Exploring the Frontiers of Aging, Metabolism and Redox Biology
Zhang, J. (2020) · Frontiers in Aging · doi:10.3389/fragi.2020.610406 · Cited by 4
“Additionally, a judicious inhibition of mitochondrial respiration may be required for activation of survival pathways (Chouchani et al., 2013).”
BackgroundBioenergetics of the Exocrine Pancreas: Physiology to Pathophysiology
Criddle, D. N. (2021) · doi:10.3998/panc.2020.17 · Cited by 4
Günther, M., Paczia, N., Michels, S., Fiebich, B. L., Vogt, S., Drewe, J., Boonen, G., Butterweck, V., & Culmsee, C. (2025) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2025.118130 · Cited by 4
Acetylation in Cardiac Aging: Molecular Mechanism and Therapeutic Approaches
Hase, A. D., & Banerjee, S. (2025) · Results and problems in cell differentiation · doi:10.1007/978-3-031-91459-1_9 · Cited by 3
Endo, Y., Takegawa, R., Murphy, M. P., Becker, L. B., & Hayashida, K. (2025) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2025.08.021 · Cited by 3
Self-citationChinopoulos, C. (2026) · Redox Biology · doi:10.1016/j.redox.2026.104224 · Cited by 3
“…pool is highly reduced in a RET-permissive configuration, localized ROS signals are generated at complex I [13] and are detected as cysteine-centered PTMs on respiratory proteins; targeted cysteine modification of complex I in turn alters ETC reactivation and downstream ROS output [107], [108].”
An injectable hydrogen-producing bacteria hydrogel for cardiac repair in rodent and porcine models
Luo, L., Xiao, Y., 劳乔聪, Ai, J., Zhou, X., Wang, G., Ma, Y., Hu, S., Zhu, D., Zhang, J., et al. (2026) · Nature Biomedical Engineering · doi:10.1038/s41551-026-01700-z · Cited by 3
Wehrle, C. J., Panconesi, R., Satish, S., Maspero, M., Jiao, C., Sun, K., Karakaya, O. F., Allkushi, E., Esfeh, J. M., Linganna, M. W., et al. (2024) · Cancers · doi:10.3390/cancers16162789 · Cited by 3
“These mechanisms are not unique to liver transplantation, and also mediate damage in myocardial infarction, stroke, and numerous other situations where tissue ischemia is induced [42].”
BackgroundZhang, M., Tan, F.-Q., Yang, J.-R., & Yu, J. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1472971 · Cited by 3
“…myocardial IRI in crush syndrome might be related to nitric oxide-mediated cytoprotection, such as the reduction of reactive oxygen species production, regulation of Ca 2+ channels, and attenuation of systemic in fl ammation (Chouchani et al., 2013; Sun et al., 2007; Sun and Murphy, 2010).”
BackgroundRETRACTED: Novel Insights Into the Role of Mitochondria-Derived Peptides in Myocardial Infarction
Wu, D., Kampmann, E., & Qian, G. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.750177 · Cited by 3
RetractedWater route for proton pumping in mitochondrial complex I
Galkin, A. S. (2020) · Nature Structural & Molecular Biology · doi:10.1038/s41594-020-0500-y · Cited by 3
Mitochondrial Disorders Due to Mutations in the Nuclear Genome
Chinnery, P. F. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-410529-4.00024-3 · Cited by 3
Responses and adaptations of cellular metabolism to temperature
Hickey, T., Harford, A. R., & Devaux, J. B. L. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-90801-6.00158-0 · Cited by 3
Cysteine redoxome landscape in the liver of male mice fed a high-fat high-sucrose diet
Galicia‐Medina, C. M., Oo, H. K., Nishiuchi, T., Tanida, R., Abuduyimiti, T., Goto, H., Nakano, Y., Takeshita, Y., Ishii, K., Toyama, T., et al. (2025) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2025.110730 · Cited by 2
“The reversible oxidation products of cysteine thiol oxidation includes the formation of disulfide bonds (S-S) (26), S-sulfenylation (S-OH) (27), S-nitrosylation (S-NO) (28), and S-gluta-thionylation (S-SG) (29).”
Metabolic pattern changes of macrophages during cancer development and progression
Liu, G., Wang, B., Wang, S., Shi, L., Han, H., & An, T. (2026) · Journal of Translational Medicine · doi:10.1186/s12967-026-08210-1 · Cited by 2
“3) [180–183].”
The Mitochondrion: A Physiological Target of Nitrite
Guimarães, D. A., Reyes, C., & Shiva, S. (2017) · Springer eBooks · doi:10.1007/978-3-319-46189-2_5 · Cited by 2
Structural Studies of Respirasome by Cryo-Electron Microscopy
Jeon, T. J., Kim, H. M., & Ryu, S. E. (2018) · Han-guk hyeonmigyeong hakoeji/Applied microscopy · doi:10.9729/am.2018.48.4.81 · Cited by 2
“In addition, it is known to be protected by the S-nitrosation of the cysteine switch (Chouchani et al., 2013).”
BackgroundNADPH oxidases, nuclear factor kappa B, NF-E2-related factor2, and oxidative stress in diabetes
Berȩsewicz, A. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-815776-3.00013-9 · Cited by 2
Vetter, T. A., Parthiban, P., Stevens, J. A., Revelo, X. S., Kohr, M. J., & Townsend, D. (2024) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2024.03.004 · Cited by 2
Wang, H., Cheng, L.-N., Zang, L., Li, B., Li, Z.-P., He, L., Zhu, Z.-F., & Yang, J. (2024) · ACS Applied Nano Materials · doi:10.1021/acsanm.4c02297 · Cited by 2
Far red/near infrared light-induced cardioprotection under normal and diabetic conditions
Keszler, Á., Baumgardt, S. L., Hwe, C., & Bienengraeber, M. (2015) · Proceedings of SPIE, the International Society for Optical Engineering/Proceedings of SPIE · doi:10.1117/12.2079880 · Cited by 2
Nitrite as Direct S-Nitrosylating Agent of Kir2.1 Channels
Montesanti, G., Parisella, M. L., Garofalo, G., & Pellegrino, D. (2014) · International Scholarly Research Notices · doi:10.1155/2014/517126 · Cited by 2
“For example, several studies have highlighted the nitrosylation mechanisms at mitochondrial level underlying the cytoprotective effects exerted by both nitrite and NO [11, 12].”
BackgroundIdentifying Single S-Nitrosothiol Sites With Cardioprotection
Anand, P., Hess, D. T., & Stamler, J. S. (2013) · Circulation Research · doi:10.1161/circresaha.113.302332 · Cited by 2
“tion against post-I/R injury in the myocardial I/R model used by Chouchani et al.(24) The results of Chouchani et al(24) also point to the impor-”
Yu, E., Calvert, P. A., Mercer, J. R., Harrison, J. B., Baker, L. L., Figg, N. L., Kumar, S., Wang, J. J., Hurst, L. A., Obaid, D. R., et al. (2014) · Circulation · doi:10.1161/circulationaha.113.008032 · Cited by 2
Self-citationMitochondrial Bioenergetics in the Heart
Lesnefsky, E. J., Chen, Q., Tandler, B., & Hoppel, C. L. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809657-4.99831-4 · Cited by 2
Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammationPreprint
Peruzzotti‐Jametti, L., Willis, C. M., Hamel, R., Krzak, G., Reisz, J. A., Prag, H. A., Wu, V., Xiang, Y., van den Bosch, A. M. R., Nicaise, A. M., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.01.03.574059 · Cited by 2
Self-citationA metabolic and mitochondrial angle on aging
Duarte, A. I., Sadowska‐Bartosz, I., Karkucińska‐Więckowska, A., Lebiedzińska, M., Palmeira, C. M., Rolo, A. P., Kabiri, Y., Zavan, B., Pinton, P., Borges, F., et al. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823761-8.00024-0 · Cited by 3
Lee, C. S., Grba, D. N., Wright, J. J., Ivanov, B. S., & Hirst, J. (2025) · Science Advances · doi:10.1126/sciadv.adz0693 · Cited by 1
Stevenson, E. R., O’Brien, J. P., Manuel, A. M., Uvalle, C. E., Buchan, G. J., Mullett, S. J., Lockwood, K. C., Suber, T. L., Freeman, B. Α., & Gelhaus, S. L. (2025) · Frontiers in Physiology · doi:10.3389/fphys.2025.1426102 · Cited by 1
“…inhibit mitochondrial oxidative respiration via the nitrosation of complex I constituents, including nicotinamide adenine dinucleotide (NAD)H-binding catalytic module components, and promote competitive inhibition of complex IV (Chouchani et al., 2013; Clementi et al., 1998; Bailey et al., 2019).”
Arabie, D. A., & Hand, S. C. (2025) · Journal of Experimental Zoology Part A Ecological and Integrative Physiology · doi:10.1002/jez.70051 · Cited by 1
Blue LEDs get the Nobel Prize while Red LEDs are poised to save lives
Karam, B. S., & Akar, F. G. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00443 · Cited by 1
“Moreover, NO reduces mitochondrial ROS levels and oxidative stress during IR injury by trapping superoxide and eliciting conformational changes that promote S-nitrosation of Complex I of the electron transport chain (Wink et al., 1993; Paolocci et al., 2001; Chouchani et al., 2013).”
BackgroundLee, G., Lee, Y. J., & Park, H. (2017) · InTech eBooks · doi:10.5772/67255 · Cited by 1
“Reversible S-nitrosation of complex I slows the reactivation of mitochondria during the crucial first minutes of the reperfusion, thereby decreasing ROS production, oxidative damage, and tissue necrosis [48].”
BackgroundNitric oxide functions in the heart
Kıvrak, T., Erdem, K., & Karaca, I. (2017) · Archives of Anatomy and Physiology · doi:10.17352/aap.000007 · Cited by 1
Arabie, D. A., Moncrief, O. G., Shirmer, S. M., & Hand, S. C. (2025) · Journal of Comparative Physiology B · doi:10.1007/s00360-025-01631-2 · Cited by 1
“Chouchani et al. (2013) confirmed that not only was the A/D transition a relevant in situ mechanism, but that the selective S -nitrosation of a critical cysteine residue of the ND3 subunit of Complex I during ischemia could prolong the reactivation of Complex I after reperfusion.”
InfluentialGuerra, D. D., Truebridge, I., Eyles, S. J., Treffon, P., & Vierling, E. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-7695-9_12 · Cited by 1
MECHANISMS OF REACTIVE OXYGEN SPECIES PRODUCTION UPON PERMEABILIZATION OF MITOCHONDRIAL MEMBRANES
Kharechkina, E. S., & Nikiforova, A. B. (2018) · Современные проблемы науки и образования · doi:10.17513/spno.27719 · Cited by 2
Commentary: A (Mito)SNO storm to protect the heart
Narahari, A. K., & Mehaffey, J. H. (2021) · JTCVS Open · doi:10.1016/j.xjon.2021.08.022 · Cited by 1
“The S-nitrosation provides protection by limiting the entry of electrons from NADH into the respiratory chain, thereby limiting the damage of reactive oxygen species during the reperfusion phase of ischemiareperfusion injury commonly seen in cardiac surgeries.(3) Preventing the reactivation of mitochondrial complex-I…”
BackgroundThe principal mitochondrial K + uniport is associated with respiratory complex IPreprint
Zemel, M. B., Angelin, A., Potluri, P., Wallace, D. C., & Fieni, F. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.01.06.475251 · Cited by 1
Respiration | Respiratory Chain Complex I
Brandt, U., & Zickermann, V. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-819460-7.00092-x · Cited by 1
Cobley, J. N. (2025) · Preprints.org · doi:10.20944/preprints202507.2120.v1 · Cited by 5
NO2- Mediates the Heart Protection of Remote Ischemic Preconditioning
Mohamed, M. S. A. (2015) · MOJ Clinical & Medical Case Reports · doi:10.15406/mojcr.2015.02.00024
Hoose, P. M. V. (2015) · ThinkIR: The University of Louisville's Institutional Repository (University of Louisville) · doi:10.18297/etd/2293
NO2- Mediates the Heart Protection of Remote Ischemic Preconditioning.
Mohamed, M. S. A. (2016) · PubMed Central
LIN28/let-7 Axis as a Regulator of Myocardial Ischemic Injury
Joshi, S. (2016)
Glutathione peroxidase in acute coronary syndromes
Holley, A. (2016) · Figshare · doi:10.26686/wgtn.17014508.v1
Chapter 25 Protection from Cardiac Ischemia and Reperfusion Injury
Bienengraeber, M. (2016) · Pan Stanford Publishing Pte. Ltd. eBooks · doi:10.1201/9781315364827-26
Reactive Oxygen Species Are Involved in Myocardial Remote Ischemic Preconditioning
Donato, M., Páez, D. T., Evelson, P., & Gelpi, R. J. (2016) · Springer eBooks · doi:10.1007/978-3-319-45865-6_17
Mohamed, M. S. A. (2017) · Journal of Vascular Medicine & Surgery · doi:10.4172/2329-6925.1000301
“This attenuates the increased production of ROS in response to IRI, and indirectly improves the functionality of complex II [28,29].”
BackgroundOBSOLETE: Mitochondria Bioenergetics in the Heart
Hoppel, C. L. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.99831-3
Structure and Function of Respiratory Complex I
Zickermann, V. (2017) · Royal Society of Chemistry eBooks · doi:10.1039/9781788010405-00060
Szívvédelem szervetlen nitrátokkal
Végh, Á., Demeter‐Haludka, V., Kovács, M. J., & Miskolczi, G. (2017) · Cardiologia Hungarica · doi:10.26430/chungarica.2017.47.sug.56
Miskolczi, G. (2018) · SZTE Repository of Dissertations (University of Szeged) · doi:10.14232/phd.4187
The Effect of Anoxia on Mitochondrial Function in a Hibernator (Ictidomys tridecemlineatus)
Hayward, L. (2018) · Scholarship@Western (Western University)
Tools for Probing and Perturbing Mitochondrial Biology
Jean, S. R. (2017) · TSpace (University of Toronto)
Cerebrovascular Dysfunction and Degeneration in Alzheimer’s Disease Pathophysiology
Quintana, D. D. (2020) · The Research Repository @ WVU (West Virginia University) · doi:10.33915/etd.7941
Therapeutic implications of targeting antioxidants to mitochondria
Víctor, V. M., Vezza, T., Apostolova, N., & Rocha, M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-85666-9.00010-3
刘巧芝, Chen, M., & 曹雪亚 (2010) · Journal of Jiaxing University
Glutathione peroxidase in acute coronary syndromes
Holley, A. (2016) · Open Access Victoria University of Wellington | Te Herenga Waka (Figshare) · doi:10.26686/wgtn.17014508
“Dysfunctional mitochondrial ROS production has been linked to early atherosclerotic lesion development [64], and the site where electrons enter the ETC is reported to be critically involved in the oxidative burst observed during ischemia/reperfusion damage [65].”
BackgroundLinden, B. (2013) · British Journal of Cardiac Nursing · doi:10.12968/bjca.2013.8.8.365
Netea, M. G., & Domínguez‐Andrés, J. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.736126018.793562936
(2015) · Assay and Drug Development Technologies · doi:10.1089/adt.2014.1507.abstracts
Mitochondrial disorders due to mutations in the nuclear genome
Chinnery, P. F., & Horváth, R. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-813955-4.00028-3
Cardioprotection with inorganic nitrites
Demeter‐Haludka, V. (2019) · SZTE Repository of Dissertations (University of Szeged) · doi:10.14232/phd.10172
(2017) · ISRN Physiology · doi:10.1155/9031
Role of fibrinogen in the attenuation of ischemia reperfusion and remote ischemic preconditioning
Mohamed, M. S. A. (2022) · Revista Colombiana de Cardiología · doi:10.24875/rccar.m22000145
Enrichment of preservation solution with methane
Szilágyi, Á. L. (2021) · doi:10.14232/phd.10969
Parmar, H. S., Tripathi, V., Jaiswal, P., Sahu, K., Majumder, S. K., Kashyap, D., Dixit, A. K., & Jha, H. C. (2022) · SSRN Electronic Journal · doi:10.2139/ssrn.4118479
Machine learning prediction and statistical analysis of redox modifications in proteins
Keßler, M. (2022) · Publication Server of Goethe University Frankfurt am Main (Goethe University Frankfurt) · doi:10.21248/gups.64467
Skolik, R. (2022) · ThinkIR: The University of Louisville's Institutional Repository (University of Louisville) · doi:10.18297/etd/3837
Kogan, M. J., Salazar-Cornejo, F., Gajardo, A. I. J., & Rodrigo, R. (2023) · BENTHAM SCIENCE PUBLISHERS eBooks · doi:10.2174/9789815165012123010011
Mitochondrial disorders due to mutations in the nuclear genome
Chinnery, P. F., & Horváth, R. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-19041-4.00055-8
Role of SDH in Cardiovascular Disorders
Patil, V. M., Masand, N., Krishnamurthy, P. T., & Gupta, S. P. (2025) · Springer eBooks · doi:10.1007/978-981-96-6831-1_6
Respiratory complex III 2 assembles complex I via toxic intermediate in mitochondrial diseasePreprint
Ayala-Hernandez, M. G., Torales, A. B., Tan, H. C., Montgomery, C. B., Padavannil, A., Cortopassi, G. A., & Letts, J. A. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.17.660237
Cobley, J. N. (2025) · Preprints.org · doi:10.20944/preprints202507.2120.v2
徐, 竟. (2025) · Advances in Clinical Medicine · doi:10.12677/acm.2025.1582375
Симутис, И. С., Lobachenko, I. G., Semigolovskii, N. Y., Danilov, M. S., Yusupov, E., Suvorova, J. V., Sapegin, A. A., Lytochkina, S. V., & Yakovlev, A. Y. (2025) · Russian Journal of Anesthesiology and Reanimatology · doi:10.17116/anaesthesiology202505188
Protective Effects on the Cardiovascular System
Chang, Z., Gu, J., & Li, X. (2025) · Springer eBooks · doi:10.1007/978-981-95-2824-0_7
Chen, Q., Li, L., Thompson, J., Hu, Y., Willard, B. B., & Lesnefsky, E. J. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.168127
Metadata
- Authors
- Chouchani, E. T., Methner, C., Nadtochiy, S. M., Logan, A., Pell, V. R., Ding, S., James, A. M., Cochemé, H. M., Reinhold, J., Lilley, K. S., Partridge, L., Fearnley, I. M., Robinson, A. J., Hartley, R. C., Smith, R. A. J., Krieg, T., Brookes, P. S., & Murphy, M. P.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- Max Planck Society (DE)
- Corresponding author
- Murphy, Michael P
- ORCID
- Venue
- Nature Medicine
- Published
- 2013-05-26
- Volume
- 19
- Issue
- 6
- Pages
- 753-759
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4019998
- OpenAlex
- W1994270731
- Semantic Scholar
- 97e1eb3beeba3f16e5a83fa5a94d80446f1bb0b7
- Cited by
- 619
- References
- 46
- Citations by year
- 2026: 19 · 2025: 38 · 2024: 39 · 2023: 31 · 2022: 42 · 2021: 51 · 2020: 59 · 2019: 37 · 2018: 60 · 2017: 50 · 2016: 60 · 2015: 54 · 2014: 58 · 2013: 20
- FWCI
- 47.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- UEA Digital Repository (University of East Anglia) (submittedVersion)
- Funders
- Wellcome Trust (098565)
- British Heart Foundation (PG/12/42/29655)
- Canadian Institutes of Health Research
- Biotechnology and Biological Sciences Research Council (BB/I012923/1, BB/I012826/1, BB/I012923)
- National Heart, Lung, and Blood Institute (R01HL071158)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- S-nitrosylation, mitochondrial complex I, nitric oxide donors, myocardial ischemia-reperfusion injury, cardioprotection, reactive oxygen species, oxidative damage, mitochondrial respiratory chain, myocardial infarction, stroke
- MeSH terms
- Animals, Cysteine, Male, Mice, Inbred C57BL, Mitochondria, Heart, Myocardial Reperfusion Injury, Nitrosation, Reactive Oxygen Species, Protein Subunits, Mitochondrial Proteins, Electron Transport Complex I, Mice, Rats
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