Acetyltransferase p300 is a putative epidrug target for amelioration of cellular aging-related cardiovascular disease

Asish K. Ghosh*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


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. Acetyl-transferase 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.

Original languageEnglish (US)
Article number2839
Issue number11
StatePublished - Nov 2021


  • Acetyltransferase p300
  • Cellular senescence
  • Diabetes
  • Heart disease
  • Hypertension
  • Small molecule inhibitors
  • TGF-β
  • Vascular calcification

ASJC Scopus subject areas

  • Medicine(all)


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