ReviewCells2022
HIV-Related Myocardial Fibrosis: Inflammatory Hypothesis and Crucial Role of Immune Cells Dysregulation.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The influence of HIV infection on myocardial fibrosis diagnosed by cardiac magnetic resonance imaging in adults: a systematic review and meta-analysis of observation studies.Frontiers in cardiovascular medicine · 2025Pooled it
- Higher plasma kynurenine-tryptophan ratio predicts incident hepatic fibrosis in women with HIV.AIDS (London, England) · 2026Article
- Association Between HIV Infection Duration and Left Ventricular Concentric Remodeling and Myocardial Fibrosis: A Cross-Sectional Study Using Cardiac MRI.Journal of magnetic resonance imaging : JMRI · 2026Article
- Editorial for "Association Between HIV Infection Duration and Left Ventricular Concentric Remodeling and Myocardial Fibrosis: A Cross-Sectional Study Using Cardiac MRI".Journal of magnetic resonance imaging : JMRI · 2026Article
- Article
- Integrated NEK7-inflammasome and platelet transcriptomic signature generates mechanistic hypotheses in heart failure.PloS one · 2026Article
- HIV, Inflammation, and Immunometabolism: A Model of the Inflammatory Theory of Disease.Viruses · 2025Review
- Double, double toil and trouble: transforming growth factor beta (TGF-β) in HIV infection.Frontiers in immunology · 2025Review
- Association Between Left Ventricular Diastolic Dysfunction, Systemic Inflammation, and Gastrointestinal Symptoms in HIV-Positive Patients on Antiretroviral Therapy.Diseases (Basel, Switzerland) · 2024Article
- PKG1 promotes the HIV-induced proliferation, migration, and fibrosis of vascular smooth muscle cells of hemorrhoids.International journal of colorectal disease · 2024Article
- HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21.International journal of molecular sciences · 2024Article
- HIV-2 mediated effects on target and bystander cells induce plasma proteome remodeling.iScience · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the underlying mechanisms driving human immunodeficiency virus (HIV)-mediated cardiovascular diseases (CVD) onset and progression remain unclear, the role of chronic immune activation as a significant mediator is increasingly being highlighted. Chronic inflammation is a characteristic feature of CVD and considered a contributor to diastolic dysfunction, heart failure, and sudden cardiac death. This can trigger downstream effects that result in the increased release of pro-coagulant, pro-fibrotic, and pro-inflammatory cytokines. Subsequently, this can lead to an enhanced thrombotic state (by platelet activation), endothelial dysfunction, and myocardial fibrosis. Of note, recent studies have revealed that myocardial fibrosis is emerging as a mediator of HIV-related CVD. Together, such factors can eventually result in systolic and diastolic dysfunction, and an increased risk for CVD. In light of this, the current review article will focus on (a) the contributions of a chronic inflammatory state and persistent immune activation, and (b) the role of immune cells (mainly platelets) and cardiac fibrosis in terms of HIV-related CVD onset/progression. It is our opinion that such a focus may lead to the development of promising therapeutic targets for the treatment and management of CVD in HIV-positive patients.
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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.