ABSTRACT
Cardiovascular disease， such as coronary heart disease and acute myocardial infarction， is a leading cause of death globally. Due to the limited proliferative and regenerative capacity of adult mammalian cardiomyocytes （CMs）， any of the current therapies cannot reverse the massive loss of CMs and subsequent fibrosis resulting from cardiac injury. Mammals mainly rely on glycolysis in the embryonic stage and fatty acid oxidation after birth for energy production. Recent reports have indicated that this metabolic pattern switch is closely related to the loss of CM proliferation. In this review， we summarize the biological characteristics of CMs and advances in heart regeneration， meanwhile shed light on the important role of CMs energy metabolism in cardiac regeneration.
ABSTRACT
<p><b>BACKGROUND</b>The human immunodeficiency virus-1 (HIV-1) envelope glycoprotein gp120 has been implicated in the development of AIDS-associated retinopathy. The present study tested the hypothesis that gp120 may induce oxidative stress including up regulation of inducible nitric oxide synthase (iNOS) and production of malondialdehyde (MDA) and nitric oxide (NO) to mediate retinopathy in retinal pigment epithelial (RPE) cells.</p><p><b>METHODS</b>Human RPE cell line D407 was cultured and treated with gp120. HIV-1 gp120 protein induced lipid peroxidation product MDA. NO production and iNOS expression were examined in vitro by spectrophomtometry, real-time PCR, Western blotting, and confocal microscope.</p><p><b>RESULTS</b>Addition of gp120 was able to induce RPE cells to produce NO and MDA in time- and dose-dependent manners (P < 0.05). Similarly, gp120 was also capable of up-regulating iNOS mRNA and protein in D407 cells in time- and dose-dependent manners.</p><p><b>CONCLUSIONS</b>Gp120 induces oxidative stress in D407 cell by stimulating MDA and NO production, which is mediated by up-regulating iNOS expression. Gp120 may mediate oxidation stress in AIDS-associated retinopathy.</p>