Nitrite as a mediator of ischemic preconditioning and cytoprotection
Open accessAbstract
Ischemia/reperfusion (IR) injury is a central component in the pathogenesis of several diseases and is a leading cause of morbidity and mortality in the western world. Subcellularly, mitochondrial dysfunction, characterized by depletion of ATP, calcium-induced opening of the mitochondrial permeability transition pore, and exacerbated reactive oxygen species (ROS) formation, plays an integral role in the progression of IR injury. Nitric oxide (NO) and more recently nitrite (NO(2)(-)) are known to modulate mitochondrial function, mediate cytoprotection after IR and have been implicated in the signaling of the highly protective ischemic preconditioning (IPC) program. Here, we review what is known about the role of NO and nitrite in cytoprotection after IR and consider the putative role of nitrite in IPC. Focus is placed on the potential cytoprotective mechanisms involving NO and nitrite-dependent modulation of mitochondrial function.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
Nitrite could be an effective source of NO in cytoprotection because it is an ample source of NO bioactivity and can be bioactivated in ischemic conditions.
“Nitrite could be an effective source of NO in cytoprotection due to its role an ample source of NO bioactivity and ability to be bioactivated in ischemic conditions [116].”
From Mechanisms of nitrite bioactivation (2014) · cites this paper as [116]
NO deficiency is associated with impaired mitochondrial function.
“Emerging evidence suggests that NO deficiency is associated with impaired mitochondrial function”
From Inorganic nitrite supplementation for healthy arterial aging (2014) · cites this paper as [135]
Restoration of NO bioavailability induces mitochondrial biogenesis.
“and that restoration of NO bioavailability induces mitochondrial biogenesis (127, 135, 167, 168)”
From Inorganic nitrite supplementation for healthy arterial aging (2014) · cites this paper as [135]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 158 · Cited by 57
- Authors
- Murillo, D., Kamga, C., Mo, L., & Shiva, S.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Shiva, Sruti
- ORCID
- Venue
- Nitric Oxide
- Publisher
- Elsevier BV
- Published
- 2011-08
- Volume
- 25
- Issue
- 2
- Pages
- 70-80
- ISSN
- 1089-8603 (ISSN-L)
- PMC
- PMC3118399
- OpenAlex
- W2044871388
- Cited by
- 57
- References
- 158
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 2 · 2015: 6 · 2014: 7 · 2013: 8 · 2012: 5
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nitric Oxide (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL096973)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- nitrite, ischemic preconditioning, ischemia-reperfusion injury, cytoprotection, mitochondrial dysfunction, mitochondrial permeability transition pore, reactive oxygen species, ATP depletion, calcium signaling
- MeSH terms
- Mitochondrial Permeability Transition Pore, Animals, Glutathione, Humans, Mitochondria, Nitric Oxide, Nitrites, Protein Processing, Post-Translational, Ubiquinone, Signal Transduction, Reperfusion Injury, Reactive Oxygen Species, Nitric Oxide Synthase, Ischemic Preconditioning, Cytoprotection, Mitochondrial Proton-Translocating ATPases, Mitochondrial Membrane Transport Proteins, Cytochromes c, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
