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HAART drugs induce mitochondrial damage and intercellular gaps and gp120 causes apoptosis

Milan Fiala1, Thomas Murphy, James MacDougall

  • 1Department of Medicine, Greater Los Angeles VA Medical Center, Los Angeles, CA, USA.

Cardiovascular Toxicology
|November 9, 2004
PubMed

Insights

Human immunodeficiency virus (HIV-1) and its proteins cause heart cell death and damage mitochondria. Highly active antiretroviral therapy (HAART) drugs also harm heart cells and blood vessels.

Area of Science:

  • Cardiovascular Science
  • Infectious Diseases
  • Toxicology

Background:

  • HIV-1 infection is linked to cardiovascular issues, but the specific roles of the virus, its proteins, and treatments like HAART are unclear.
  • While HAART reduces heart disease risk, it can cause metabolic problems and potentially coronary artery disease.

Purpose of the Study:

  • To investigate the toxic effects of HIV-1, HIV-1 glycoprotein 120 (gp120), and HAART drugs on heart and endothelial cells.
  • To understand the mechanisms behind HIV-1 and HAART-related cardiovascular complications.

Main Methods:

  • Assessed apoptosis in neonatal rat ventricular myocytes (NRVMs) and human coronary artery endothelial cells (CAECs) exposed to HIV-1, gp120, and azidothymidine (AZT).
  • Examined mitochondrial damage in cardiomyocytes.
  • Measured intercellular gaps and transendothelial electrical resistance in endothelial cells treated with HAART drugs.

Main Results:

  • HIV-1 and gp120 induced apoptosis in NRVMs and CAECs, while AZT did not.
  • Ethylisothiourea, a nitric oxide synthase inhibitor, reduced gp120-induced apoptosis.
  • AZT, HIV-1, and gp120 damaged cardiomyocyte mitochondria.
  • HAART drugs (AZT, indinavir) created gaps in endothelial cells and reduced electrical resistance.

Conclusions:

  • HIV-1 and gp120 directly cause cardiomyocyte and endothelial cell apoptosis, contributing to cardiovascular toxicity.
  • HAART medications can disrupt endothelial cell structure and mitochondria, potentially leading to vascular damage.

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