ReviewFrontiers in immunology2025
HIV-Tat and vascular endothelium: implications in the HIV associated brain, heart, and lung complications.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Metabolic dysfunction-associated steatotic liver disease in people living with HIV: mechanisms, diagnosis, and management.Frontiers in immunology · 2026Review
- Beyond Viral Assembly: The Emerging Role of HIV-1 p17 in Vascular Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- Contrasting cannabinoid receptor 2 (CB2R)-mediated responses in two different models of Blood Brain Barrier in the context of HIV.Research square · 2025Article
- HIV-1 Tat Protein Exposure Alters the Morphological Characteristics and Gene Expression in the Primary Mouse Cortex Endothelial Cells and Human Brain Microvascular Endothelial Cells.Cellular and molecular neurobiology · 2025Article
- The Role of Toll-like Receptors and Viral Infections in the Pathogenesis and Progression of Pulmonary Arterial Hypertension-A Narrative Review.International journal of molecular sciences · 2025Review
- HIV-1 Tat protein exposure alters the morphological characteristics and gene expression in the primary mouse cortex endothelial cells and human brain microvascular endothelial cells.Research square · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Following the advent of antiretroviral therapy (ART), neurological, cardiovascular, and pulmonary comorbidities emerged as major challenges in treating non-infectious complications in people living with HIV. Despite effective ART, HIV viral proteins can persist in circulation even in individuals with negligible viral loads, potentially contributing to cellular and tissue-level stress, inflammation, and related health complications. Most of the HIV protein: Tat (Trans activator of Transcription), expressed in HIV-infected cells, is actively secreted and exerts its pathological effects on non-infected cells, particularly impacting the vascular endothelium. This review focuses on the role and the underlying mechanisms of HIV-Tat in promoting endothelial dysfunction across the cardiovascular, pulmonary, and brain vasculature. Additionally, we discuss how HIV-Tat interacts synergistically with drugs of abuse to exacerbate endothelial damage. Importantly, the vascular damage caused by Tat is not fully mitigated by HAART, necessitating further mechanistic investigations and targeted therapeutic interventions. Additionally, cessation of drug abuse is indispensable for improving clinical outcomes and restoring vascular health in people living with HIV.
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Registered trials
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