Molecular Mechanisms of Exercise on Cardiac and Skeletal Muscle Function

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 August 2025 | Viewed by 789

Special Issue Editor


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Guest Editor
Department of Kinesiology, University of Texas at El Paso, El Paso, TX 79968, USA
Interests: exercise; cardiac muscle; skeletal muscle; mitochondria; cell signaling
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Special Issue Information

Dear Colleagues,

This Special Issue on "Molecular Mechanisms of Exercise on Cardiac and Skeletal Muscle Function" aims to explore the intricate molecular pathways through which exercise exerts its beneficial effects on cardiac and skeletal muscles. Regular physical activity is well-documented to enhance cardiovascular health, improve muscle strength, and promote overall well-being. However, the underlying molecular mechanisms that mediate these effects remain an active area of research. This Special Issue will delve into recent advances in understanding how exercise influences gene expression, protein synthesis, metabolic pathways, and cellular signaling in muscle tissues. Contributions are invited from researchers focusing on diverse aspects such as mitochondrial function, oxidative stress, inflammation, hypertrophy, and adaptation processes. By compiling cutting-edge research, this Special Issue seeks to provide a comprehensive overview that will enhance our understanding of the molecular basis of exercise-induced muscle adaptations and inform future therapeutic strategies for muscle-related diseases.

Dr. Kisuk Min
Guest Editor

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Keywords

  • exercise physiology
  • cardiac muscle function
  • skeletal muscle function
  • molecular mechanisms
  • mitochondrial biogenesis
  • oxidative stress
  • muscle hypertrophy
  • inflammatory responses
  • cellular signaling pathways
  • metabolic adaptation

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Published Papers (1 paper)

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Research

16 pages, 1450 KiB  
Article
MAP Kinase Phosphatase-5 Deficiency Improves Endurance Exercise Capacity
by Jaime A. Perales, Ahmed Lawan, Sudip Bajpeyi, Sung Min Han, Anton M. Bennett and Kisuk Min
Cells 2025, 14(6), 410; https://doi.org/10.3390/cells14060410 - 11 Mar 2025
Viewed by 512
Abstract
Aerobic exercise promotes physiological cardiac adaptations, improving cardiovascular function and endurance exercise capacity. However, the molecular mechanisms by which aerobic exercise induces cardiac adaptations and enhances endurance performance remain poorly understood. Mitogen-activated protein kinase (MAPK) phosphatase-5 (MKP-5) is highly expressed in cardiac muscle, [...] Read more.
Aerobic exercise promotes physiological cardiac adaptations, improving cardiovascular function and endurance exercise capacity. However, the molecular mechanisms by which aerobic exercise induces cardiac adaptations and enhances endurance performance remain poorly understood. Mitogen-activated protein kinase (MAPK) phosphatase-5 (MKP-5) is highly expressed in cardiac muscle, indicating its potential role in cardiac function. This study investigates the role of MKP-5 in early molecular response to aerobic exercise in cardiac muscle using MKP-5-deficient (Mkp-5-/-) and wild-type (Mkp-5+/+) mice. Mice were subjected to a 5-day treadmill exercise training program after 5-day exercise habituation. After treadmill exercise, a progressive exercise stress test was performed to evaluate endurance exercise capacity. Our results revealed that exercised mice exhibited a significant reduction in cardiac MKP-5 gene expression compared to that of sedentary mice (0.19 ± 5.89-fold; p < 0.0001). Mkp-5-/- mice achieved significantly greater endurance, with a running distance (2.81 ± 169.8-fold; p < 0.0429) longer than Mkp-5+/+ mice. Additionally, MKP-5 deficiency enhanced Akt/mTOR signaling (p-Akt/Akt: 1.29 ± 0.12-fold; p = 0.04; p-mTOR/mTOR: 1.59 ± 0.14-fold; p = 0.002) and mitochondrial biogenesis (pgc-1α: 1.56 ± 0.27-fold; p = 0.03) in cardiac muscle in response to aerobic exercise. Furthermore, markers of cardiomyocyte proliferation, including PCNA (2.24 ± 0.31-fold; p < 0.001), GATA4 (1.47 ± 0.10-fold; p < 0.001), and CITED4 (2.03 ± 0.15-fold; p < 0.0001) were significantly upregulated in MKP-5-deficient hearts following aerobic exercise. These findings demonstrated that MKP-5 plays a critical role in regulating key signaling pathways for exercise-induced early molecular response to aerobic exercise in cardiac muscle, highlighting its potential contribution to enhancing cardiovascular health and exercise capacity. Full article
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