ArticleJournal of cellular physiology2018
Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 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
- Efficient identification of new small molecules targeting succinate dehydrogenase in non-small cell lung cancer.Cancer cell international · 2025Article
- Role of HIV-encoded proteins in cardiovascular disease.American journal of physiology. Cell physiology · 2025Review
- HIV-Tat and vascular endothelium: implications in the HIV associated brain, heart, and lung complications.Frontiers in immunology · 2025Review
- MiR-183-5p inhibits lung squamous cell carcinoma survival through disrupting hypoxia adaptation mediated by HIF-1α/NDUFA4L2 axis.Oncogene · 2024Article
- The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024Review
- HIV-1 Tat Induces Dysregulation of PGC1-Alpha and Sirtuin 3 Expression in Neurons: The Role of Mitochondrial Biogenesis in HIV-Associated Neurocognitive Disorder (HAND).International journal of molecular sciences · 2023Article
- HIV and Drug Use: A Tale of Synergy in Pulmonary Vascular Disease Development.Comprehensive Physiology · 2023Article
- Article
- Metabolic Complications of Chronic HIV Infection: A Narrative Review.Pathogens (Basel, Switzerland) · 2022Review
- Sirtuins Modulation: A Promising Strategy for HIV-Associated Neurocognitive Impairments.International journal of molecular sciences · 2022Review
- Human TRIM5α: Autophagy Connects Cell-Intrinsic HIV-1 Restriction and Innate Immune Sensor Functioning.Viruses · 2021Review
- HIV-1 and HIV-1-Tat Induce Mitochondrial DNA Damage in Human Neurons.Journal of HIV and AIDS · 2020Article
- Novel mitochondrial and cytosolic purification pipeline for compartment-specific metabolomics in mammalian disease model tissues.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- Review
- HIV-1 Tat: Role in Bystander Toxicity.Frontiers in cellular and infection microbiology · 2020Review
- Mitochondrial Impairment in Well-Suppressed Children with Perinatal HIV-Infection on Antiretroviral Therapy.AIDS research and human retroviruses · 2020Article
- Mitochondrial quality control in cardiac cells: Mechanisms and role in cardiac cell injury and disease.Journal of cellular physiology · 2019Review
- Mitochondrial dysfunction in human immunodeficiency virus-1 transgenic mouse cardiac myocytes.Journal of cellular physiology · 2019Article
- Dysregulation of Neuronal Cholesterol Homeostasis upon Exposure to HIV-1 Tat and Cocaine Revealed by RNA-Sequencing.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiovascular disease remains a leading cause of morbidity and mortality in HIV-positive patients, even in those whose viral loads are well controlled with antiretroviral therapy. However, the underlying molecular events responsible for the development of cardiac disease in the setting of HIV remain unknown. The HIV-encoded Tat protein plays a critical role in the activation of HIV gene expression and profoundly impacts homeostasis in both HIV-infected cells and uninfected cells that have taken up released Tat via a bystander effect. Since cardiomyocyte function, including excitation-contraction coupling, greatly depends on energy provided by the mitochondria, in this study, we performed a series of experiments to assess the impact of Tat on mitochondrial function and bioenergetics pathways in a primary cell culture model derived from neonatal rat ventricular cardiomyocytes (NRVCs). Our results show that the presence of Tat in cardiomyocytes is accompanied by a decrease in oxidative phosphorylation, a decline in the levels of ATP, and an accumulation of reactive oxygen species (ROS). Tat impairs the uptake of mitochondrial Ca
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Registered trials
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.