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ERK1/2: An Integrator of Signals That Alters Cardiac Homeostasis and Growth

期刊

BIOLOGY-BASEL
卷 10, 期 4, 页码 -

出版社

MDPI
DOI: 10.3390/biology10040346

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ERK; extracellular matrix; heart; cardiac hypertrophy

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资金

  1. NIH [HL136951, HL154001]

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Understanding how cardiac cells respond to external stimuli through the ERK1/2 pathway is crucial for maintaining heart health and responding to stress. The review highlights the complexity of upstream and downstream signals involved in ERK1/2-dependent regulation, particularly focusing on cardiomyocyte hypertrophy as an outcome of ERK1/2 activation regulation in the heart.
Simple Summary Understanding how cardiac cells respond to external stimuli is essential for developing interventions that mitigate pathologies of the heart. Therefore, in this review, we summarize critical knowledge related to a key molecular pathway that mediates cellular responses. Integration of cellular responses to extracellular cues is essential for cell survival and adaptation to stress. Extracellular signal-regulated kinase (ERK) 1 and 2 serve an evolutionarily conserved role for intracellular signal transduction that proved critical for cardiomyocyte homeostasis and cardiac stress responses. Considering the importance of ERK1/2 in the heart, understanding how these kinases operate in both normal and disease states is critical. Here, we review the complexity of upstream and downstream signals that govern ERK1/2-dependent regulation of cardiac structure and function. Particular emphasis is given to cardiomyocyte hypertrophy as an outcome of ERK1/2 activation regulation in the heart.

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