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. 2022 Jul 18;23(14):7916. doi: 10.3390/ijms23147916

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Pathological mechanisms of VSMC hypertrophy. Angiotensin II (AngII) leads to phosphorylation of HDAC4/5 chaperone 14-3-3 binding sites through CaMKII-dependent (HDAC4) and CaMKII-independent (HDAC5) mechanisms. Under physiological conditions, HDAC4/5 forms complexes with myocyte enhancer factor-2 (MEF2). Under pathological conditions, complex formation is downregulated and MEF2 leads to activation of hypertrophic genes for contractile proteins such as beta-MHC, atrial natriuretic factor (ANF), and transcription factor KLF5, leading to VSMC hypertrophy.