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Histone deacetylase 6 inhibition attenuates pathological cardiac hypertrophy by promoting autophagy through MAP1LC3B

Jiayu Yao1, Xiaoou Sun2, Yousheng Chen1

  • 1School of Life Science and Technology, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, PR China.

The Journal of Pathology
|April 11, 2025
PubMed

Insights

Histone deacetylase 6 (HDAC6) drives pathological cardiac hypertrophy by inhibiting autophagy. This occurs through interaction with and ubiquitination of MAP1LC3B, reducing its levels and impairing heart function.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Pathophysiology

Background:

  • Cardiac hypertrophy is a maladaptive heart response leading to dysfunction and heart failure.
  • Histone deacetylase 6 (HDAC6) is implicated in cardiovascular diseases.
  • Autophagy dysregulation contributes to myocardial hypertrophy, but HDAC6's role is unknown.

Purpose of the Study:

  • To investigate the role of HDAC6 in pathological cardiac hypertrophy.
  • To elucidate the mechanism by which HDAC6 affects cardiac hypertrophy, specifically its link to autophagy.

Main Methods:

  • Utilized isoproterenol (ISO)-induced cardiac hypertrophy models in vitro and in vivo.
  • Assessed HDAC6 expression and its impact on hypertrophic gene expression and cell size.
  • Examined the interaction between HDAC6 and MAP1LC3B (Microtubule-associated protein 1A/1B-light chain 3B).
  • Investigated the effect of HDAC6 inhibition on autophagy and hypertrophic markers.

Main Results:

  • HDAC6 expression was upregulated in ISO-induced cardiac hypertrophy.
  • HDAC6 overexpression exacerbated hypertrophy, while inhibition attenuated it.
  • HDAC6 negatively regulated autophagy by interacting with and ubiquitinating MAP1LC3B, reducing its levels.
  • HDAC6 inhibition restored MAP1LC3B levels and improved autophagy in hypertrophic hearts.

Conclusions:

  • HDAC6 plays a critical role in pathological cardiac hypertrophy.
  • HDAC6 promotes cardiac hypertrophy by suppressing autophagy via MAP1LC3B ubiquitination.
  • Targeting HDAC6 may offer a therapeutic strategy for cardiac hypertrophy.

Keywords:
HDAC6ISOMAP1LC3Bautophagycardiac hypertrophyubiquitination

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