Cross-talk between L-type Ca2+ channels and mitochondria
- PMID: 19671062
- DOI: 10.1111/j.1440-1681.2009.05277.x
Cross-talk between L-type Ca2+ channels and mitochondria
Abstract
1. Calcium is necessary for myocardial function, including contraction and maintenance of cardiac output. Calcium is also necessary for myocardial energetics and production of ATP by mitochondria, but the mechanisms for calcium regulation by mitochondria are still not fully resolved. 2. The cytoskeleton plays an important role in maintaining a cell's integrity. It is now recognized that cytoskeletal proteins can also assist in the transmission of signals from the plasma membrane to intracellular organelles. Cytoskeletal proteins can regulate the function of the L-type Ca(2+) channel and alter intracellular calcium homeostasis. 3. Recent evidence suggests that calcium influx through the L-type Ca(2+) channel is sufficient to alter a number of mitochondrial functional parameters, including superoxide production, NADH production and metabolic activity, assessed as the formation of formazan from tetrazolium salt. This occurs in a calcium-dependent manner. 4. Activation of the L-type Ca(2+) channel also alters mitochondrial membrane potential in a calcium-independent manner and this is assisted by movement of the auxiliary beta(2)-subunit through F-actin filaments. 5. Because the L-type Ca(2+) channel is the initiator of contraction, a functional coupling between the channels and mitochondria may assist in meeting myocardial energy demand on a beat-to-beat basis.
Similar articles
-
The L-type Ca(2+) channel facilitates abnormal metabolic activity in the cTnI-G203S mouse model of hypertrophic cardiomyopathy.J Physiol. 2016 Jul 15;594(14):4051-70. doi: 10.1113/JP271681. Epub 2016 Jun 12. J Physiol. 2016. PMID: 27062056 Free PMC article.
-
How does calcium regulate mitochondrial energetics in the heart? - new insights.Heart Lung Circ. 2014 Jul;23(7):602-9. doi: 10.1016/j.hlc.2014.02.009. Epub 2014 Feb 28. Heart Lung Circ. 2014. PMID: 24657282 Review.
-
Evidence for regulation of mitochondrial function by the L-type Ca2+ channel in ventricular myocytes.J Mol Cell Cardiol. 2009 Jun;46(6):1016-26. doi: 10.1016/j.yjmcc.2008.12.015. Epub 2009 Jan 7. J Mol Cell Cardiol. 2009. PMID: 19166857
-
The L-type Ca(2+) channel as a potential mediator of pathology during alterations in cellular redox state.Heart Lung Circ. 2009 Feb;18(1):3-10. doi: 10.1016/j.hlc.2008.11.004. Epub 2008 Dec 31. Heart Lung Circ. 2009. PMID: 19119068 Review.
-
Transient exposure to hydrogen peroxide causes an increase in mitochondria-derived superoxide as a result of sustained alteration in L-type Ca2+ channel function in the absence of apoptosis in ventricular myocytes.Circ Res. 2007 Apr 13;100(7):1036-44. doi: 10.1161/01.RES.0000263010.19273.48. Epub 2007 Mar 8. Circ Res. 2007. PMID: 17347474
Cited by
-
A maladaptive feedback mechanism between the extracellular matrix and cytoskeleton contributes to hypertrophic cardiomyopathy pathophysiology.Commun Biol. 2023 Jan 3;6(1):4. doi: 10.1038/s42003-022-04278-9. Commun Biol. 2023. PMID: 36596888 Free PMC article.
-
Mitochondrial Function and Dysfunction in Dilated Cardiomyopathy.Front Cell Dev Biol. 2021 Jan 12;8:624216. doi: 10.3389/fcell.2020.624216. eCollection 2020. Front Cell Dev Biol. 2021. PMID: 33511136 Free PMC article. Review.
-
Characterization and validation of a preventative therapy for hypertrophic cardiomyopathy in a murine model of the disease.Proc Natl Acad Sci U S A. 2020 Sep 15;117(37):23113-23124. doi: 10.1073/pnas.2002976117. Epub 2020 Aug 28. Proc Natl Acad Sci U S A. 2020. PMID: 32859761 Free PMC article.
-
Structure of the MICU1-MICU2 heterodimer provides insights into the gatekeeping threshold shift.IUCrJ. 2020 Feb 27;7(Pt 2):355-365. doi: 10.1107/S2052252520001840. eCollection 2020 Mar 1. IUCrJ. 2020. PMID: 32148862 Free PMC article.
-
GRKs and β-Arrestins: "Gatekeepers" of Mitochondrial Function in the Failing Heart.Front Pharmacol. 2019 Feb 12;10:64. doi: 10.3389/fphar.2019.00064. eCollection 2019. Front Pharmacol. 2019. PMID: 30809146 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous