Adrenergic Receptor Regulation of Mitochondrial Function in Cardiomyocytes.
Journal
Journal of cardiovascular pharmacology
ISSN: 1533-4023
Titre abrégé: J Cardiovasc Pharmacol
Pays: United States
ID NLM: 7902492
Informations de publication
Date de publication:
01 09 2022
01 09 2022
Historique:
received:
28
10
2021
accepted:
01
02
2022
pubmed:
17
2
2022
medline:
9
9
2022
entrez:
16
2
2022
Statut:
epublish
Résumé
Adrenergic receptors (ARs) are G protein-coupled receptors that are stimulated by catecholamines to induce a wide array of physiological effects across tissue types. Both α1- and β-ARs are found on cardiomyocytes and regulate cardiac contractility and hypertrophy through diverse molecular pathways. Acute activation of cardiomyocyte β-ARs increases heart rate and contractility as an adaptive stress response. However, chronic β-AR stimulation contributes to the pathobiology of heart failure. By contrast, mounting evidence suggests that α1-ARs serve protective functions that may mitigate the deleterious effects of chronic β-AR activation. Here, we will review recent studies demonstrating that α1- and β-ARs differentially regulate mitochondrial biogenesis and dynamics, mitochondrial calcium handling, and oxidative phosphorylation in cardiomyocytes. We will identify potential mechanisms of these actions and focus on the implications of these findings for the modulation of contractile function in the uninjured and failing heart. Collectively, we hope to elucidate important physiological processes through which these well-studied and clinically relevant receptors stimulate and fuel cardiac contraction to contribute to myocardial health and disease.
Identifiants
pubmed: 35170492
doi: 10.1097/FJC.0000000000001241
pii: 00005344-202209000-00006
pmc: PMC9365878
mid: NIHMS1779348
doi:
Substances chimiques
Adrenergic beta-Agonists
0
Receptors, Adrenergic, alpha-1
0
Receptors, Adrenergic, beta
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
364-377Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL140067
Pays : United States
Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
Déclaration de conflit d'intérêts
The authors report no conflicts of interest.
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