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Complement factor D derived from epicardial adipose tissue participates in cardiomyocyte apoptosis after myocardial

Shuang Hao1, Jingchao Zhang1, Yu Pei1

  • 1Department of Cardiac Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, China.

Cellular Signalling
|November 9, 2022
PubMed

Insights

Epicardial adipose tissue (EAT) secretes complement factor D (CFD) after myocardial infarction (MI), promoting cardiomyocyte apoptosis via PARP-1 activation. Inhibiting CFD alleviates this damage, offering a potential therapeutic target for heart failure post-MI.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pathophysiology

Background:

  • Acute myocardial infarction (MI) is a primary cause of congestive heart failure.
  • Understanding the underlying pathophysiological processes is crucial for developing interventions.

Purpose of the Study:

  • To analyze the pathophysiological mechanisms of acute MI.
  • To identify key therapeutic targets for MI-induced heart failure.

Main Methods:

  • Established a rat model of MI by ligating the left anterior descending branch.
  • Collected heart, epicardial adipose tissue (EAT), and subcutaneous adipose tissue (SAT).
  • Utilized H9c2 cells to investigate the role of complement factor D (CFD) in cardiomyocyte apoptosis.

Main Results:

  • MI rats exhibited myocardial apoptosis and increased EAT.
  • EAT-conditioned medium reduced H9c2 cell activity.
  • Elevated CFD in EAT promoted cardiomyocyte apoptosis via PARP-1 activation, which was reversed by CFD inhibition (CFD-IN1).

Conclusions:

  • Epicardial adipose tissue (EAT) mediates cardiomyocyte apoptosis following MI.
  • CFD secretion by EAT and subsequent PARP-1 activation are key mechanisms.
  • Inhibition of CFD presents a potential therapeutic strategy for MI.
Abstract

Keywords:
CFDCardiomyocyte apoptosisEATMyocardial infarctionPARP-1

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