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Oxygen Radicals Released During Ischemic Preconditioning Contribute to Cardioprotection in the Rabbit Myocardium
Abstract
Previous studies have proposed that oxygen radicals may play a role in the triggering of ischemic preconditioning. However, studies evaluating the effects of radical scavengers have yielded conflicting results, possibly because of differences in the number of preconditioning episodes used. The present study tested whether N-2-mercaptopropionylglycine (MPG) could block protection of both single and multiple episodes of preconditioning in in situ and in vitro rabbit hearts. All hearts were subjected to 30 min of regional ischemia followed by reperfusion for 2 (in vitro) or 3 (in situ) h. Infarct size was measured by tetrazolium. Infarction in control in situ hearts was 37.5+/-3.5% of the risk zone. A single cycle of preconditioning (PC1), with 5 min ischemia/10 min reperfusion, reduced infarct size to 12.3+/-2.0% (P<0.05). Four cycles of preconditioning (PC4) were equally protective. MPG (1 mg/kg/min i.v.) alone had no effect on infarction but abolished protection afforded by PC1 (35.4+/-3.9%). However, MPG failed to block protection in the PC4 group. In isolated control hearts, infarct size was 31.1+/-1.8% and was reduced to 10.2+/-2.2% (P<0.05) by preconditioning. MPG (300 microM) aborted protection. Infusion of hypoxanthine or xanthine oxidase separately in lieu of preconditioning had no effect on infarct size, but induced protection when combined (14.1+/-2.2%; P<0.05). Polymyxin B, an inhibitor of protein kinase C (PKC), abolished this protection (53.1+/-4.1%). In conclusion, oxygen radicals contribute to ischemic preconditioning in the rabbit and appear to do so via activation of PKC. The fact that MPG could not block protection by PC4 suggests that oxygen radicals act in concert with other triggers of preconditioning such as adenosine and bradykinin.
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“Although constitutively expressed, the HIF-1α subunit has a very short half-life in normoxic conditions because of its rapid hydroxylation by prolyl-4 hydroxylases (PH1–3) (12, 36).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [12]
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Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury
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“PKC ε also appears to be activated by the ROS generated during the brief preconditioning cycles of ischemia and reperfusion (15).”
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“In contrast to our own data suggesting that IPC exerts its effects on the MPTP indirectly, Baines et al. [44] have very recently provided evidence that PKCq may interact directly with VDAC to cause its phosphorylation and consequent inhibition of MPTP opening.”
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YELLON, D. M., & DOWNEY, J. M. (2003) · Physiological Reviews · doi:10.1152/physrev.00009.2003 · Cited by 1,062
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Cadenas, S. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.01.024 · Cited by 832
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Hypoxia induces severe right ventricular dilatation and infarction in heme oxygenase-1 null mice
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Forbes, R. A., Steenbergen, C., & Murphy, E. (2001) · Circulation Research · doi:10.1161/hh0801.089342 · Cited by 395
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“For example, during cardiac ischemic preconditioning, in a ROS-dependent mechanism, brief ischemic periods of ischemia can induce protection against cell damage during longer ischemia–reperfusion [8,9].”
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D’Oria, R., Schipani, R., Leonardini, A., Natalicchio, A., Perrini, S., Cignarelli, A., Laviola, L., & Giorgino, F. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/5732956 · Cited by 399
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Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review
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“Interestingly, the same mechanisms, generation of ROS and activation of PKC, have been proposed to play a role in ischaemic preconditioning (Baines et al. 1997; Vanden Hoek et al. 1998; Pain et al. 2000).”
BackgroundSignaling pathways in ischemic preconditioning
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Preconditioning in Cardiomyocytes Protects by Attenuating Oxidant Stress at Reperfusion
Hoek, T. L. V., Becker, L. B., Shao, Z., Li, C., & Schumacker, P. T. (2000) · Circulation Research · doi:10.1161/01.res.86.5.541 · Cited by 312
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Self-citationThe pH Hypothesis of Postconditioning
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Self-citationPreconditioning and postconditioning: United at reperfusion
Hausenloy, D. J., & Yellon, D. M. (2007) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2007.06.005 · Cited by 285
Mechanisms of Cardioprotection by Volatile Anesthetics
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“tive effect of the preconditioning stimulus on infarct size.(161,162) These findings indicate that IPC is mediated”
BackgroundKevin, L. G., Camara, A. K. S., Riess, M. L., Novalija, E., & Stowe, D. F. (2003) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00711.2002 · Cited by 272
“Exogenous administration of H2O2 can induce a preconditioned state in cardiomyocytes (44) and intact hearts (43), and a similar effect can be achieved by endogenous ROS formation by the xanthine/xanthine oxidase reaction (4, 52) or by using the ETC inhibitor menadione (49).”
BackgroundMethodInfluentialCaspase 3 activation is essential for neuroprotection in preconditioning
McLaughlin, B., Hartnett, K. A., Erhardt, J. A., Legos, J. J., White, R. F., Barone, F. C., & Aizenman, E. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0232966100 · Cited by 271
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“Anti-inflammatory ? Possibly [10,12] Inhibits PMN and endothelial cell activation Superoxide anions Yes [98] Signaling Yes [97,99,100] Increased mitochondrial ROS Possibly Mitochondrial? Oxidative ‘‘burst’’ Yes [100] Yes [12,13] Decreased generation; [10,12,13,41] Increased endogenous antioxidants [33] Protein kinase…”
BackgroundIsoform-Selective Activation of Protein Kinase C by Nitric Oxide in the Heart of Conscious Rabbits
Ping, P., Takano, H., Zhang, J., Tang, X., Qiu, Y., Li, R. C. X., Banerjee, S., Dawn, B., Balafonova, Z., & Bolli, R. (1999) · Circulation Research · doi:10.1161/01.res.84.5.587 · Cited by 254
Mitochondrial Ion Channels: Gatekeepers of Life and Death
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“Baines and colleagues have suggested that dissipation of the proton gradient by KATP channel openers and mitochondrial depolarisation leads to an increase in oxidant stress [32].”
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“The ROS scavenger N-2-mercaptopropionyl glycine completely blocked the cardioprotection induced by an IPC stimulus consisting of 5 min ischaemia followed by 10 min reperfusion in rabbit.(6,7) Moreover, modest concentrations of free radicals are sufficient to induce protection in the heart.”
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Heme oxygenase and carbon monoxide initiate homeostatic signaling
Bilban, M., Haschemi, A., Wegiel, B., Chin, B. Y., Wagner, O. F., & Otterbein, L. E. (2007) · Journal of Molecular Medicine · doi:10.1007/s00109-007-0276-0 · Cited by 245
“Although high concentrations of CO are toxic (as are all substances) and while there is excessive production of ROS by the mitochondria, inhibition of oxidative phosphorylation, and the generation of adenosine triphosphate (ATP) [46], recent reports continue to support that this generation of ROS at nondetrimental amo…”
BackgroundHermes‐Lima, M., Moreira, D. C., Rivera‐Ingraham, G. A., Giraud‐Billoud, M., Genaro‐Mattos, T. C., & Campos, E. G. (2015) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2015.07.156 · Cited by 246
“…through indirect means, such as through the use of antioxidants (which reduce the cardioprotective effects of IPC) (Tanaka et al. 1994) and prooxidants (which under normoxia induced IPC-like protection as shown by Baines et al. (Baines, 1997) or Vanden Hoek et al. (Vanden Hoek et al., 1998)).”
ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel
Lebuffe, G., Schumacker, P. T., Shao, Z.-H., Anderson, T., Iwase, H., & Vanden Hoek, T. L. (2003) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00706.2002 · Cited by 227
“We (42) and others (1, 2, 41) have found that oxidant signals contribute to hypoxia-induced preconditioning.”
BackgroundCardioprotection: A radical view
Penna, C. R. R., Mancardi, D., Rastaldo, R., & Pagliaro, P. (2009) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2009.02.008 · Cited by 225
“[107] and Tritto et al.”
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“[81] showed that a free radical scavenger could block preconditioning induced by one or more short ischemic episodes.”
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“Finally, diazoxide has been reported to increase the mitochondrial production of reactive oxygen species (ROS) by an unknown mechanism (Pain et al. 2000; Liu & O’Rourke, 2001; Forbes et al. 2001), and ROS have been implicated in IPC (Baines et al. 1997; Vanden Hoek et al. 1998).”
BackgroundOpening mitoKATPincreases superoxide generation from complex I of the electron transport chain
Andrukhiv, A., Costa, A. D. T., West, I. C., & Garlid, K. (2006) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00272.2006 · Cited by 224
“The proposal that mitoKATP opening leads to increased mitochondrial ROS production (14) is widely accepted, based in part on studies in intact cells (24, 38, 44) and in part on the effects of free radical scavengers on cardioprotection in isolated intact hearts (3, 8, 12, 40, 47, 49).”
BackgroundMitochondrial Reactive Oxygen Species at the Heart of the Matter
Kornfeld, O. S., Hwang, S., Disatnik, M., Chen, C., Qvit, N., & Mochly‐Rosen, D. (2015) · Circulation Research · doi:10.1161/circresaha.116.305432 · Cited by 215
Mitochondrial KATP channels: role in cardioprotection
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Mechanism of Cardioprotection by Early Ischemic Preconditioning
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“IPC’s protection can be mimicked by transient exposure to an oxygen radical generating system, and, conversely, a ROS scavenger can abolish protection from IPC [28, 29].”
BackgroundSelf-citationThe direct physiological effects of mitoKATPopening on heart mitochondria
Costa, A. D. T., Quinlan, C. L., Andrukhiv, A., West, I. C., Jabůrek, M., & Garlid, K. (2005) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00794.2005 · Cited by 201
“It has been known for some time that scavengers of reactive oxygen species (ROS) block cardioprotection (3, 10, 42, 44), leading Downey and coworkers (42) to propose that mitoKATP opening is a trigger of cardioprotection via mitoKATP-dependent ROS signaling.”
BackgroundMyocardial apoptosis and ischemic preconditioning.
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“Finally, diazoxide has been reported to increase the mitochondrial production of reactive oxygen species (ROS) by an unknown mechanism (Pain et al. 2000; Forbes et al. 2001; Liu & O’Rourke, 2001), and ROS have been implicated in IPC (Baines et al. 1997; Vanden Hoek et al. 1998).”
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“(135), ROS generation by the ETC (10, 240), K (cid”
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“This is borne out by the lack of effect of adenosine catabolites such as inosine and hypoxanthine on postischemic recovery (13, 227).”
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Self-citationα-Ketoglutarate dehydrogenase: A mitochondrial redox sensor
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Remote preconditioning protects the heart by activating myocardial PKCε-isoform
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Ischemic preconditioning: Exploring the paradox
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Isoflurane Preconditions Myocardium against Infarction via Release of Free Radicals
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Self-citationMechanism of Preconditioning by Isoflurane in Rabbits: A Direct Role for Reactive Oxygen Species
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“Free radical scavengers administered during ischemic preconditioning (IPC) markedly attenuate the protective effect of the preconditioning stimulus on infarct size.(5,7) These data suggest that IPC is mediated in part by small quantities of ROS released during preconditioning.”
BackgroundBudas, G. R., Churchill, E. N., & Mochly‐Rosen, D. (2007) · Pharmacological Research · doi:10.1016/j.phrs.2007.04.005 · Cited by 153
Signal Transduction in Ischemic Preconditioning:
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Self-citationOhnuma, Y., Miura, T., Miki, T., Tanno, M., Kuno, A., Tsuchida, A., & Shimamoto, K. (2002) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00434.2001 · Cited by 152
“Also, it has not been determined whether opening of the mitochondrial KATP channel is necessary for PKC activation by PC, although pharmacological evidence suggests that the role of free radicals in PC is induction of PKC activation (2).”
BackgroundEpsilon protein kinase C as a potential therapeutic target for the ischemic heart
Inagaki, K., Churchill, E. N., & Mochly‐Rosen, D. (2006) · Cardiovascular Research · doi:10.1016/j.cardiores.2006.02.015 · Cited by 150
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“It has been reported that ROS are involved in IP and that exposure to ROS generating system could precondition the heart [27,36,38,43–46].”
Krenz, M., Oldenburg, O., Wimpee, H., Cohen, M. V., Garlid, K., Critz, S. D., Downey, J. M., & Benoit, J. N. (2002) · Basic Research in Cardiology · doi:10.1007/s003950200045 · Cited by 147
Self-citationNovalija, E., Fujita, S., Kampine, J. P., et al. (1999) · Anesthesiology · doi:10.1097/00000542-199909000-00023 · Cited by 145
Ischemic preconditioning: nearly two decades of research. A comprehensive review
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“Treatment with MPG prior to an ischemic preconditioning stimulus in the rabbit heart attenuates protection against ischemia/reperfusion injury and MPG given before the ischemic insult has no effect on infarct size (Baines et al., 1997).”
BackgroundReactive Oxygen Species as Intracellular Signaling Molecules in the Cardiovascular System
Krylatov, A. V., Маслов, Л. Н., Воронков, Н. С., Boshchenko, A. A., Popov, S. V., Gomez, L., Wang, H., Jaggi, A. S., & Downey, J. M. (2018) · Current Cardiology Reviews · doi:10.2174/1573403x14666180702152436 · Cited by 144
“Depending on the concentration, oxidants play a dual role in stimulating or inactivating PKC. IPC is a phenomenon whereby a brief transient ischemic insult causes the heart to become resistant to infarction from a subsequent extended period of ischemia.”
BackgroundInfluentialSelf-citationProtection in the aged heart: preventing the heart-break of old age?
Juhaszova, M., Rabuel, C., Zorov, D. B., Lakatta, E. G., & Sollott, S. J. (2005) · Cardiovascular Research · doi:10.1016/j.cardiores.2004.12.020 · Cited by 142
“Preventing ROS-signaling (which plays an obligatory role as a trigger of PC) by ROS-scavengers can abolish PC [6,32,33].”
BackgroundReactive Oxygen Species as Mediators of Signal Transduction in Ischemic Preconditioning
Otani, H. (2004) · Antioxidants and Redox Signaling · doi:10.1089/152308604322899521 · Cited by 139
“Several independent investigators have indeed suggested the involvement of ROS or redox modulation in activating cardio-protective signal transduction pathways in IPC (13, 44, 259, 293, 295).”
cGMP signalling in pre- and post-conditioning: the role of mitochondria
Costa, A. D. T., Pierre, S. V., Cohen, M. V., Downey, J. M., & Garlid, K. (2007) · Cardiovascular Research · doi:10.1093/cvr/cvm050 · Cited by 141
“We believe that ROS produced by mitochondria act as second messengers to activate PKC through redox signalling.(17,18) ROS production is deficient in mice genetically engineered to lack connexin 43, a protein on the inner mitochondrial membrane that forms gap junctions, and this may account for the loss of IPC’s prote…”
BackgroundSelf-citationWeinbrenner, C. (2003) · Cardiovascular Research · doi:10.1016/j.cardiores.2003.10.008 · Cited by 138
“The dose of MPG was selected to 20 mg/kg body weight since other groups have demonstrated that this dose does inhibit the protection by one classical preconditioning stimulus [24, 27,28].”
BackgroundInfluentialXia, Z., Huang, Z., & Ansley, D. M. (2006) · Anesthesia & Analgesia · doi:10.1213/01.ane.0000230612.29452.a6 · Cited by 136
Tang, X., Feng, J., Chen, J., Chen, P., Zhi, J., Cui, Y., Guo, R., & Yu, H. (2005) · Brain Research · doi:10.1016/j.brainres.2005.07.072 · Cited by 136
Miki, T., Cohen, M. V., & Downey, J. M. (1998) · Molecular and Cellular Biochemistry · doi:10.1023/a:1006856124501 · Cited by 131
“Many substances are released by the myocardium during ischemia, and several of them, including adenosine [3, 4], bradykinin [5, 6] and free radicals [7, 8], act to trigger preconditioning.”
InfluentialSelf-citationRavati, A., Ahlemeyer, B., Becker, A., Klumpp, S., & Krieglstein, J. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00463.x · Cited by 130
Pasdois, P., Parker, J. E., Griffiths, E. J., & Halestrap, A. P. (2011) · Biochemical Journal · doi:10.1042/bj20101957 · Cited by 127
COHEN, M., YANG, X., & Downey, J. M. (2005) · Cardiovascular Research · doi:10.1016/j.cardiores.2005.10.021 · Cited by 128
“Thus interference with ROS production after triggering of preconditioning with ischemia can abort cardioprotection while controlled production of ROS in lieu of another preconditioning stimulus can decrease infarction [24,25].”
BackgroundSelf-citationThe paradigm of postconditioning to protect the heart
Penna, C. R. R., Mancardi, D., Raimondo, S., Geuna, S., & Pagliaro, P. (2007) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2007.00210.x · Cited by 122
“Thus the main idea was that ROS play an essential, though double-edged, role in cardioprotection: they may participate in reperfusion injury or may play a role as signalling elements of protection in pre-ischaemic phase [10, 48, 57–59, 64–68, 76, 125, 136, 138, 139, 144–147].”
BackgroundYamashita, N., Hoshida, S., Taniguchi, N., et al. (1998) · Circulation · doi:10.1161/01.cir.98.14.1414 · Cited by 124
Mitochondrial dysfunction as the cause of the failure to precondition the diabetic human myocardium
HASSOUNA, A., Loubani, M., Matata, B. M., FOWLER, A., Standen, N. B., & Galiñanes, M. (2005) · Cardiovascular Research · doi:10.1016/j.cardiores.2005.11.004 · Cited by 123
“Release of superoxide by coinfusion of hypoxanthine and xanthine oxidase elicits cardioprotection in the rabbit heart [22] while the superoxide scavenger MnTBAP abrogates ischemic protection in the guinea pig [56].”
BackgroundJoo, J. D., Kim, M., D’Agati, V. D., & Lee, H. T. (2006) · Journal of the American Society of Nephrology · doi:10.1681/asn.2006050424 · Cited by 121
Carroll, R. (2001) · Cardiovascular Research · doi:10.1016/s0008-6363(01)00330-3 · Cited by 122
Hypoxia-inducible factor as a therapeutic target for cardioprotection
Ong, S., & Hausenloy, D. J. (2012) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2012.07.005 · Cited by 113
“(1988) first demonstrated that antioxidants could abolish the protective effect elicited by IPC, implicating for the first time a role for ROS as a critical mediator of IPC, a finding which was later supported by several experimental studies (Tanaka et al., 1994; Chen et al., 1995; Baines et al., 1997).”
BackgroundResultInfluentialComplex Regulation of Mitochondrial Function During Cardiac Development
Zhao, Q., Sun, Q., Zhou, L., Liu, K., & Jiao, K. (2019) · Journal of the American Heart Association · doi:10.1161/jaha.119.012731 · Cited by 116
Xenon and Sevoflurane Protect against Brain Injury in a Neonatal Asphyxia Model
Luo, Y., Ma, D., Ieong, E., et al. (2008) · Anesthesiology · doi:10.1097/aln.0b013e3181895f88 · Cited by 110
“Protein kinase C is thought to be activated possibly by reactive oxygen spices, which are generated by preconditioning.(35) Experimental studies have implied that PKC activation is an important step in preconditioning by ischemia, xenon, and sevoflurane.”
BackgroundChen, H., Chien, C., Yu, S., Lee, Y., & Chen, W. (2002) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0704908 · Cited by 108
“Mitochondria produce and are a ected by ROS, which have been shown to paradoxically initiate both apoptosis and cardioprotection (Baines et al., 1997; Cai & Jones, 1998).”
BackgroundCohen, M. V., & Downey, J. M. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12903 · Cited by 111
“Ytrehus et al. (1994) reported that PKC seemed to play a major role in IPC and it was found that protection triggered by any of the three receptors could be blocked by PKC inhibitors (Goto et al., 1995; Sakamoto et al., 1995; Baines et al., 1997; Miki et al., 1998a).”
BackgroundSelf-citationChurchill, E. N., Disatnik, M., & Mochly‐Rosen, D. (2008) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2008.09.713 · Cited by 107
“Additionally, there are several mitochondrial targets of εPKC which protect the heart from I/ R injury through mechanisms including ROS generation [59,60], opening of the mitochondrial permeability transition pore (MPTP) [61,62], regulation of the mitochondrial kATP channels (reviewed in [63,64]) and activation of mit…”
BackgroundImmunity, Inflammation, and Oxidative Stress in Heart Failure: Emerging Molecular Targets
Ayoub, K. F., Pothineni, N. V. K., Rutland, J. J., Ding, Z., & Mehta, J. L. (2017) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-017-6752-z · Cited by 107
“preconditions the heart against subsequent episodes of severe ischemia, and antioxidant therapies may decrease this beneficial effect of preconditioning [99].”
BackgroundSánchez, G., Escobar, M., Pedrozo, Z., Macho, P., DOMENECH, R. J., Härtel, S., Hidalgo, C., & Donoso, P. (2007) · Cardiovascular Research · doi:10.1093/cvr/cvm011 · Cited by 105
Oldenburg, O. (2002) · Cardiovascular Research · doi:10.1016/s0008-6363(02)00332-2 · Cited by 105
Metadata
- Authors
- Baines, C. P., Goto, M., & Downey, J. M.
- Affiliations
- University of South Alabama (US)
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 1997-01
- Volume
- 29
- Issue
- 1
- Pages
- 207-216
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2122501550
- Cited by
- 484
- References
- 0
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 8 · 2018: 8 · 2017: 11 · 2016: 12 · 2015: 12 · 2014: 16 · 2013: 21 · 2012: 18
- FWCI
- 13.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- ischemic preconditioning, oxygen free radicals, cardioprotection, protein kinase C, infarct size, myocardial ischemia-reperfusion injury, xanthine oxidase, hypoxanthine, adenosine, bradykinin, radical scavengers
- MeSH terms
- Analysis of Variance, Animals, Enzyme Activation, Female, Free Radicals, Hemodynamics, Male, Tiopronin, Myocardial Infarction, Protein Kinase C, Rabbits, Free Radical Scavengers, Reactive Oxygen Species, Ischemic Preconditioning, Myocardial, In Vitro Techniques
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