ArticlePloS one2016
Bicarbonate Increases Ischemia-Reperfusion Damage by Inhibiting Mitophagy.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Sodium bicarbonate attenuates myocardial ischemia-reperfusion injury via activation of the splenic cholinergic anti-inflammatory pathway.JTCVS open · 2026Article
- Simulated ischaemia/reperfusion impairs trophoblast function through divergent oxidative stress- and MMP-9-dependent mechanisms.Bioscience reports · 2024Article
- Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.Nature communications · 2024Article
- Therapeutic Strategies Targeting Mitochondrial Dysfunction in Sepsis-induced Cardiomyopathy.Cardiovascular drugs and therapy · 2024Review
- Mitophagy for cardioprotection.Basic research in cardiology · 2023Review
- Review
- Resveratrol Reestablishes Mitochondrial Quality Control in Myocardial Ischemia/Reperfusion Injury through Sirt1/Sirt3-Mfn2-Parkin-PGC-1α Pathway.Molecules (Basel, Switzerland) · 2022Article
- Myocardial and mitochondrial effects of the anhydrase carbonic inhibitor ethoxzolamide in ischemia-reperfusion.Physiological reports · 2021Article
- Mitochondrial quality control mechanisms as molecular targets in cardiac ischemiaActa pharmaceutica Sinica. B · 2020Review
- Targeting mitochondrial fusion and fission proteins for cardioprotection.Journal of cellular and molecular medicine · 2020Review
- Inhibition of the ubiquitous calpains protects complex I activity and enables improved mitophagy in the heart following ischemia-reperfusion.American journal of physiology. Cell physiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
During an ischemic event, bicarbonate and CO2 concentration increase as a consequence of O2 consumption and lack of blood flow. This event is important as bicarbonate/CO2 is determinant for several redox and enzymatic reactions, in addition to pH regulation. Until now, most work done on the role of bicarbonate in ischemia-reperfusion injury focused on pH changes; although reperfusion solutions have a fixed pH, cardiac resuscitation protocols commonly employ bicarbonate to correct the profound acidosis associated with respiratory arrest. However, we previously showed that bicarbonate can increase tissue damage and protein oxidative damage independent of pH. Here we show the molecular basis of bicarbonate-induced reperfusion damage: the presence of bicarbonate selectively impairs mitophagy, with no detectable effect on autophagy, proteasome activity, reactive oxygen species production or protein oxidation. We also show that inhibition of autophagy reproduces the effects of bicarbonate in reperfusion injury, providing additional evidence in support of this mechanism. This phenomenon is especially important because bicarbonate is widely used in resuscitation protocols after cardiac arrest, and while effective as a buffer, may also contribute to myocardial injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.