Kv beta complex facilitates exercise-induced augmentation of myocardial perfusion and cardiac growth.

Autor:	Raph SM; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Calderin EP; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Nong Y; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Brittian K; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Garrett L; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Zhang D; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States., Nystoriak MA; Center for Cardiometabolic Science, Department of Medicine, Division of Environmental Medicine, University of Louisville, Louisville, KY, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2024 Jun 24; Vol. 11, pp. 1411354. Date of Electronic Publication: 2024 Jun 24 (Print Publication: 2024).
DOI:	10.3389/fcvm.2024.1411354
Abstrakt:	The oxygen sensitivity of voltage-gated potassium (Kv) channels regulates cardiovascular physiology. Members of the Kv1 family interact with intracellular Kvβ proteins, which exhibit aldo-keto reductase (AKR) activity and confer redox sensitivity to Kv channel gating. The Kvβ proteins contribute to vasoregulation by controlling outward K + currents in smooth muscle upon changes in tissue oxygen consumption and demand. Considering exercise as a primary physiological stimulus of heightened oxygen demand, the current study tested the role of Kvβ proteins in exercise performance, exercise-induced adaptations in myocardial perfusion, and physiological cardiac growth. Our findings reveal that genetic ablation of Kvβ2 proteins diminishes baseline exercise capacity in mice and attenuates the enhancement in exercise performance observed after long-term training. Moreover, we demonstrate that Kvβ2 proteins are critical for exercise-mediated enhancement in myocardial perfusion during cardiac stress as well as adaptive changes in cardiac structure. Our results underscore the importance of Kvβ proteins in metabolic vasoregulation, highlighting their role in modulating both exercise capacity and cardiovascular benefits associated with training. Furthermore, our study sheds light on a novel molecular target for enhancing exercise performance and improving the health benefits associated with exercise training in patients with limited capacity for physical activity. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (© 2024 Raph, Calderin, Nong, Brittian, Garrett, Zhang and Nystoriak.)
Databáze:	MEDLINE
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