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Prohibitin overexpression improves myocardial function in diabetic cardiomyopathy

Wen-qian Dong1, Min Chao2, Qing-hua Lu3

  • 1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital, Shandong University, Jinan, China.

Oncotarget
|December 2, 2015
PubMed

Insights

Prohibitin (PHB) protein overexpression improved cardiac function in a type 2 diabetic rat model. PHB reduced insulin resistance, fibrosis, and apoptosis, suggesting it as a therapeutic target for diabetic cardiomyopathy (DCM).

Area of Science:

  • Cardiovascular Biology
  • Metabolic Diseases
  • Molecular Medicine

Background:

  • Prohibitin (PHB) is a conserved protein involved in cell proliferation, apoptosis, and mitochondrial function.
  • The role of PHB in diabetic cardiomyopathy (DCM) remains largely unknown.
  • Diabetic cardiomyopathy is characterized by insulin resistance, cardiac dysfunction, fibrosis, and apoptosis.

Purpose of the Study:

  • To investigate the role of Prohibitin (PHB) in the pathogenesis of type 2 diabetic cardiomyopathy (DCM).
  • To explore the therapeutic potential of PHB overexpression in ameliorating DCM.
  • To elucidate the molecular mechanisms underlying PHB's effects in DCM.

Main Methods:

  • A type 2 diabetic rat model was established using a high-fat diet and streptozotocin.
  • PHB overexpression was induced in vivo via lentiviral gene delivery.
  • Cardiac function was assessed using metabolic tests, echocardiography, and histopathology.
  • In vitro studies utilized cardiofibroblasts and H9c2 cardiomyoblasts under high glucose conditions.

Main Results:

  • PHB overexpression significantly ameliorated DCM symptoms, including insulin resistance, left ventricular dysfunction, fibrosis, and apoptosis.
  • In cardiofibroblasts, PHB overexpression reduced collagen expression, matrix metalloproteinase activity, and proliferation.
  • In H9c2 cardiomyoblasts, PHB overexpression inhibited high glucose-induced apoptosis.
  • PHB overexpression modulated key signaling pathways, decreasing ERK1/2 phosphorylation and restoring Akt phosphorylation.

Conclusions:

  • Prohibitin (PHB) plays a protective role in diabetic cardiomyopathy.
  • PHB overexpression demonstrates therapeutic potential for treating DCM.
  • PHB influences key cellular processes like fibrosis, apoptosis, and signaling pathways in DCM.

Keywords:
Pathology Sectionapoptosisdiabetic cardiomyopathymyocardial fibrosisprohibitin

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