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The protective role of peroxisome proliferator-activated receptor γ coactivator-1α in hyperthyroid cardiac

Wei Xu1, Dongxia Hou, Xiangrui Jiang

  • 1Jiangsu Diabetes Center, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.

Journal of Cellular Physiology
|November 23, 2011
PubMed

Insights

Triiodothyronine (T3) can cause cardiac hypertrophy, but PGC-1α offers protection. T3 reduces PGC-1α via the p38 MAPK pathway, highlighting a novel regulatory mechanism in heart disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Endocrinology

Background:

  • Heart failure is a global health concern.
  • Hyperthyroidism-induced cardiac hypertrophy contributes to heart failure.
  • The precise mechanisms of thyroid hormone action on the heart are not fully understood.

Purpose of the Study:

  • To investigate the role of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) in Triiodothyronine (T3)-induced cardiac hypertrophy.
  • To elucidate the signaling pathways involved in T3-mediated effects on PGC-1α.

Main Methods:

  • Assessed PGC-1α mRNA expression in rat hearts following T3 exposure in vivo and ex vivo.
  • Utilized small interfering RNA and overexpression techniques in cardiomyocytes to study PGC-1α function.
  • Investigated the involvement of the p38 mitogen-activated protein kinases (MAPK) pathway.

Main Results:

  • Extended T3 treatment increased PGC-1α expression, while shorter treatments decreased it.
  • Suppression of PGC-1α exacerbated T3-induced cardiomyocyte hypertrophy; PGC-1α overexpression was protective.
  • T3 reduced PGC-1α expression via the p38 MAPK pathway.
  • PGC-1α overexpression inhibited both basal and T3-induced p38 MAPK phosphorylation.

Conclusions:

  • PGC-1α plays a protective role against T3-induced cardiac hypertrophy.
  • A regulatory pathway exists between PGC-1α and p38 MAPK in T3-induced cardiac hypertrophy.

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