Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

Cardiovascular disease is the leading cause of accelerated as well as chronological aging-related human morbidity and mortality worldwide. Genetic, immunologic, unhealthy lifestyles including daily consumption of high-carb/high-fat fast food, lack of exercise, drug addiction, cigarette smoke, alcoho...

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Autor principal:	Asish K. Ghosh
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	acetyltransferase p300 small molecule inhibitors cellular senescence diabetes TGF-β vascular calcification Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/3772cc04b268423dafcf4bdc948c2364
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spelling	oai:doaj.org-article:3772cc04b268423dafcf4bdc948c23642021-11-25T17:07:46ZAcetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease10.3390/cells101128392073-4409https://doaj.org/article/3772cc04b268423dafcf4bdc948c23642021-10-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2839https://doaj.org/toc/2073-4409Cardiovascular disease is the leading cause of accelerated as well as chronological aging-related human morbidity and mortality worldwide. Genetic, immunologic, unhealthy lifestyles including daily consumption of high-carb/high-fat fast food, lack of exercise, drug addiction, cigarette smoke, alcoholism, and exposure to environmental pollutants like particulate matter (PM)-induced stresses contribute profoundly to accelerated and chronological cardiovascular aging and associated life threatening diseases. All these stressors alter gene expression epigenetically either through activation or repression of gene transcription via alteration of chromatin remodeling enzymes and chromatin landscape by DNA methylation or histone methylation or histone acetylation. Acetyltransferase p300, a major epigenetic writer of acetylation on histones and transcription factors, contributes significantly to modifications of chromatin landscape of genes involved in cellular aging and cardiovascular diseases. In this review, the key findings those implicate acetyltransferase p300 as a major contributor to cellular senescence or aging related cardiovascular pathologies including vascular dysfunction, cardiac hypertrophy, myocardial infarction, cardiac fibrosis, systolic/diastolic dysfunction, and aortic valve calcification are discussed. The efficacy of natural or synthetic small molecule inhibitor targeting acetyltransferase p300 in amelioration of stress-induced dysregulated gene expression, cellular aging, and cardiovascular disease in preclinical study is also discussed.Asish K. GhoshMDPI AGarticleacetyltransferase p300small molecule inhibitorscellular senescencediabetesTGF-βvascular calcificationBiology (General)QH301-705.5ENCells, Vol 10, Iss 2839, p 2839 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	acetyltransferase p300 small molecule inhibitors cellular senescence diabetes TGF-β vascular calcification Biology (General) QH301-705.5
spellingShingle	acetyltransferase p300 small molecule inhibitors cellular senescence diabetes TGF-β vascular calcification Biology (General) QH301-705.5 Asish K. Ghosh Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
description	Cardiovascular disease is the leading cause of accelerated as well as chronological aging-related human morbidity and mortality worldwide. Genetic, immunologic, unhealthy lifestyles including daily consumption of high-carb/high-fat fast food, lack of exercise, drug addiction, cigarette smoke, alcoholism, and exposure to environmental pollutants like particulate matter (PM)-induced stresses contribute profoundly to accelerated and chronological cardiovascular aging and associated life threatening diseases. All these stressors alter gene expression epigenetically either through activation or repression of gene transcription via alteration of chromatin remodeling enzymes and chromatin landscape by DNA methylation or histone methylation or histone acetylation. Acetyltransferase p300, a major epigenetic writer of acetylation on histones and transcription factors, contributes significantly to modifications of chromatin landscape of genes involved in cellular aging and cardiovascular diseases. In this review, the key findings those implicate acetyltransferase p300 as a major contributor to cellular senescence or aging related cardiovascular pathologies including vascular dysfunction, cardiac hypertrophy, myocardial infarction, cardiac fibrosis, systolic/diastolic dysfunction, and aortic valve calcification are discussed. The efficacy of natural or synthetic small molecule inhibitor targeting acetyltransferase p300 in amelioration of stress-induced dysregulated gene expression, cellular aging, and cardiovascular disease in preclinical study is also discussed.
format	article
author	Asish K. Ghosh
author_facet	Asish K. Ghosh
author_sort	Asish K. Ghosh
title	Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
title_short	Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
title_full	Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
title_fullStr	Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
title_full_unstemmed	Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease
title_sort	acetyltransferase p300 is a putative epidrug target for amelioration of cellular aging-related cardiovascular disease
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/3772cc04b268423dafcf4bdc948c2364
work_keys_str_mv	AT asishkghosh acetyltransferasep300isaputativeepidrugtargetforameliorationofcellularagingrelatedcardiovasculardisease
_version_	1718412706601500672

Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

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