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Rock protein as cardiac hypertrophy modulator in obesity and physical exercise. | LitMetric

Rock protein as cardiac hypertrophy modulator in obesity and physical exercise.

Life Sci

Department of Physical Education, Institute of Biosciences - São Paulo State University (UNESP), Rio Claro, SP, Brazil; Exercise Cell Biology Lab (ECEBIL), School of Applied Science - University of Campinas, Limeira, SP, Brazil; CEPECE - Center of Research in Sport Sciences, School of Applied Sciences - University of Campinas (UNICAMP), Limeira, SP, Brazil. Electronic address:

Published: August 2020

AI Article Synopsis

  • Obesity and cardiovascular diseases are major global health concerns, with ROCK protein playing a significant role in cardiac hypertrophy by affecting leptin and insulin signaling pathways.
  • * Leptin activates ROCK, which increases MAPK activity and disrupts insulin signaling, contributing to abnormal heart growth, while physical exercise helps reduce leptin levels and improve insulin signaling, promoting healthier heart development.
  • * More research is needed to understand the different isoforms of ROCK and their impact in the context of exercise and obesity, as this could lead to better treatment strategies for cardiovascular issues.

Article Abstract

Obesity and cardiovascular diseases are worldwide public health issues. In this review, we discussed the participation of ROCK protein in cardiac hypertrophy, mainly through the modulation of leptin and insulin signaling pathways. Leptin plays a role in cardiovascular disease development and, through the Rho-associated protein kinase (ROCK), promotes cardiac hypertrophy. ROCK protein, is regulated by small Rho-GTPases and has two isoforms with high homology. ROCK is able to activate the MAP kinase (MAPK) pathway and modulate insulin signaling in the heart, participating in cardiac hypertrophy development of concentric and eccentric left ventricle growth. Although different types of stimulus can lead to morphologically antagonistic heart growth, physical exercise promotes improvements in hemodynamic function, emerging as a promising non-pharmacological tool to improve overall health. Leptin can activate ROCK in a pathological way, increasing MAPK activity and decreasing insulin signaling via insulin receptor substrate 1 (IRS1) serine 307 residue phosphorylation, phosphatase and tensin homolog, and protein kinase Cβ2. In turn, physical exercise decreases leptin levels and positively modulates insulin signaling as well as increases ROCK-dependent IRS1 (Ser632/635) phosphorylation, improving phosphatidylinositol 3-kinase/protein kinase B axis and promoting physiologic heart growth. Currently, there is a lack of studies about differences in ROCK isoforms, especially during exercise and/or obesity. However, the understanding of its biological function and the complex mechanism underlying the distinct types of cardiac hypertrophy development can be a useful tool in the improvement and treatment of cardiovascular outcomes.

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Source
http://dx.doi.org/10.1016/j.lfs.2019.116955DOI Listing

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