Mitochondrial depolarization and the role of uncoupling proteins in ischemia tolerance
- PMID: 16914124
- DOI: 10.1016/j.cardiores.2006.07.010
Mitochondrial depolarization and the role of uncoupling proteins in ischemia tolerance
Abstract
Modest depolarization of the mitochondrial inner membrane potential is known to attenuate mitochondrial reactive oxygen species generation. Transient pharmacologic uncoupling of mitochondrial oxidative phosphorylation results in modest depolarization of the mitochondrial membrane potential and confers protection against subsequent cardiac ischemia-reperfusion injury. Whether cardiac mitochondria have an innate capacity to temporally self-modulate their membrane potential as a possible adaptive mechanism in the context of cardiac ischemia and early reperfusion is supported by emerging data and is an intriguing concept that warrants further investigation. The objective of this review is to explore the various mechanisms whereby mitochondrial depolarization can be evoked in the context of both cardiac ischemia and reperfusion and in response to the cardioprotective program of ischemic preconditioning. The potential regulatory pathways orchestrating this biological perturbation of mitochondrial function are explored from the level of signal transduction to potential transcription-mediated modulations of nuclear-encoded mitochondrial inner membrane proteins, emphasizing the potential function of the mitochondrial uncoupling proteins.
Similar articles
-
Transient mitochondrial permeability transition pore opening mediates preconditioning-induced protection.Circulation. 2004 Apr 13;109(14):1714-7. doi: 10.1161/01.CIR.0000126294.81407.7D. Epub 2004 Apr 5. Circulation. 2004. PMID: 15066952
-
Mitochondria and ischemia/reperfusion injury.Ann N Y Acad Sci. 2005 Jun;1047:248-58. doi: 10.1196/annals.1341.022. Ann N Y Acad Sci. 2005. PMID: 16093501 Review.
-
The mitochondrial biogenesis regulatory program in cardiac adaptation to ischemia--a putative target for therapeutic intervention.Trends Cardiovasc Med. 2005 Apr;15(3):118-23. doi: 10.1016/j.tcm.2005.05.001. Trends Cardiovasc Med. 2005. PMID: 16039972 Review.
-
Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion.Am J Physiol Cell Physiol. 2007 Jan;292(1):C137-47. doi: 10.1152/ajpcell.00270.2006. Epub 2006 Sep 13. Am J Physiol Cell Physiol. 2007. PMID: 16971498 Review.
-
Mitochondrial respiration and membrane potential after low-flow ischemia are not affected by ischemic preconditioning.J Mol Cell Cardiol. 2007 Nov;43(5):610-5. doi: 10.1016/j.yjmcc.2007.08.004. Epub 2007 Aug 17. J Mol Cell Cardiol. 2007. PMID: 17884086
Cited by
-
The Multifaceted Functions of TRPV4 and Calcium Oscillations in Tissue Repair.Int J Mol Sci. 2024 Jan 18;25(2):1179. doi: 10.3390/ijms25021179. Int J Mol Sci. 2024. PMID: 38256251 Free PMC article. Review.
-
Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia/reperfusion injury.Cardiovasc Res. 2023 Oct 24;119(13):2342-2354. doi: 10.1093/cvr/cvad120. Cardiovasc Res. 2023. PMID: 37556386 Free PMC article.
-
MitoQ as an antenatal antioxidant treatment improves markers of lung maturation in healthy and hypoxic pregnancy.J Physiol. 2023 Aug;601(16):3647-3665. doi: 10.1113/JP284786. Epub 2023 Jul 19. J Physiol. 2023. PMID: 37467062 Free PMC article.
-
Mitochondrial protective effects caused by the administration of mefenamic acid in sepsis.J Neuroinflammation. 2022 Nov 4;19(1):268. doi: 10.1186/s12974-022-02616-6. J Neuroinflammation. 2022. PMID: 36333747 Free PMC article.
-
Uncoupling protein 1 knockout aggravates isoproterenol-induced acute myocardial ischemia via AMPK/mTOR/PPARα pathways in rats.Transgenic Res. 2022 Feb;31(1):107-118. doi: 10.1007/s11248-021-00289-0. Epub 2021 Oct 28. Transgenic Res. 2022. PMID: 34709566 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources