ArticleProceedings of the National Academy of Sciences of the United States of America2002
Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion- and death receptor-controlled pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 114 citations in OpenAlex.
- HIV heart inflammation is mediated by HIV infected myeloid cells, HIV-tat secretion, and aberrant function of Connexin43-containing channels.Scientific reports · 2026Article
- Molecular insights in HIV-associated cardiac dysfunction.Communications medicine · 2025Article
- Cardiac MRI in Identifying Myopericarditis Mimicking STEMI in a Patient with HIV: A Case Report.The American journal of case reports · 2025Article
- Cardiovascular Disease in HIV Patients: A Comprehensive Review of Current Knowledge and Clinical Implications.International journal of molecular sciences · 2025Review
- HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21.International journal of molecular sciences · 2024Article
- Electrocardiographic abnormalities and associated factors among HIV-infected adults on antiretroviral therapy.Frontiers in reproductive health · 2024Article
- Multimodality Imaging in HIV-Associated Cardiovascular Complications: A Comprehensive Review.International journal of environmental research and public health · 2023Review
- A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023Review
- A Comprehensive Outlook on Dilated Cardiomyopathy (DCM): State-Of-The-Art Developments with Special Emphasis on OMICS-Based Approaches.Journal of cardiovascular development and disease · 2022Review
- Incidence of cardiovascular diseases in a nationwide HIV/AIDS patient cohort in Taiwan from 2000 to 2014.Epidemiology and infection · 2018Article
- Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes.Journal of cellular physiology · 2018Article
- HIV Proteins and Endothelial Dysfunction: Implications in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2018Review
- HIV-1 Nef-induced cardiotoxicity through dysregulation of autophagy.Scientific reports · 2017Article
- The Causes of HIV-Associated Cardiomyopathy: A Tale of Two Worlds.BioMed research international · 2016Review
- Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016Review
- A Novel Role of Proline Oxidase in HIV-1 Envelope Glycoprotein-induced Neuronal Autophagy.The Journal of biological chemistry · 2015Article
- Human Immunodeficiency Virus and Heart Failure in Low- and Middle-Income Countries.JACC. Heart failure · 2015Review
- CCR5 inhibition prevents cardiac dysfunction in the SIV/macaque model of HIV.Journal of the American Heart Association · 2014Article
- HIV-1 subtype C unproductively infects human cardiomyocytes in vitro and induces apoptosis mitigated by an anti-Gp120 aptamer.PloS one · 2014Article
- Myocardial infarction caused by pharmacological substances - case description and literature review.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2013Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
We investigated 18 AIDS hearts (5 with and 13 without cardiomyopathy) by using immunocytochemistry and computerized image analysis regarding the roles of HIV-1 proteins and tumor necrosis factor ligands in HIV cardiomyopathy (HIVCM). HIVCM and cardiomyocyte apoptosis were significantly related to each other and to the expression by inflammatory cells of gp120 and tumor necrosis factor-alpha. In HIVCM heart, active caspase 9, a component of the mitochondrion-controlled apoptotic pathway, and the elements of the death receptor-mediated pathway, tumor necrosis factor-alpha and Fas ligand, were expressed strongly on macrophages and weakly on cardiomyocytes. HIVCM showed significantly greater macrophage infiltration and cardiomyocyte apoptosis rate compared with non-HIVCM. HIV-1 entered cultured neonatal rat ventricular myocytes by macropinocytosis but did not replicate. HIV-1- or gp120-induced apoptosis of rat myocytes through a mitochondrion-controlled pathway, which was inhibited by heparin, AOP-RANTES, or pertussis toxin, suggesting that cardiomyocyte apoptosis is induced by signaling through chemokine receptors. In conclusion, in patients with HIVCM, cardiomyocytes die through both mitochondrion- and death receptor-controlled apoptotic pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.