ArticleThe Journal of clinical investigation1998
HIV-1 kills renal tubular epithelial cells in vitro by triggering an apoptotic pathway involving caspase activation and Fas upregulation.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 154 citations in OpenAlex.
- Interruption of antiretroviral therapy is associated with increased plasma cystatin C.AIDS (London, England) · 2009Trial
- Polymyxin-B hemoperfusion inactivates circulating proapoptotic factors.Intensive care medicine · 2008Trial
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- NEF-Induced HIV-Associated Nephropathy Through HCK/LYN Tyrosine Kinases.The American journal of pathology · 2023Article
- Ameliorative effect of chitosan nanoparticles against carbon tetrachloride-induced nephrotoxicity in Wistar rats.Pharmaceutical biology · 2022Article
- Reduced Thiamine Availability and Hyperglycemia Impair Thiamine Transport in Renal Glomerular Cells through Modulation of Thiamine Transporter 2.Biomedicines · 2021Article
- Increased proportion of apoptotic cells in cat kidney tissues infected with feline morbillivirus.Archives of virology · 2020Article
- Acute Tubular Injury is Associated With Severe Traumatic Brain Injury: in Vitro Study on Human Tubular Epithelial Cells.Scientific reports · 2019Observational
- Effects of linagliptin on human immortalized podocytes: a cellular system to study dipeptidyl-peptidase 4 inhibition.British journal of pharmacology · 2017Article
- Soluble CD40 ligand directly alters glomerular permeability and may act as a circulating permeability factor in FSGS.PloS one · 2017Article
- HIV infection-induced transcriptional program in renal tubular epithelial cells activates a CXCR2-driven CD4+ T-cell chemotactic response.AIDS (London, England) · 2016Article
- Update on current management of chronic kidney disease in patients with HIV infection.International journal of nephrology and renovascular disease · 2016Review
- Infection-Related Focal Segmental Glomerulosclerosis in Children.BioMed research international · 2016Review
- Cardiorenal Syndrome Type 1: Activation of Dual Apoptotic Pathways.Cardiorenal medicine · 2015Article
- Histamine receptor expression in human renal tubules: a comparative pharmacological evaluation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- HIV-associated nephropathies: epidemiology, pathology, mechanisms and treatment.Nature reviews. Nephrology · 2015Review
- Cardiorenal syndrome type 5: in vitro cytotoxicity effects on renal tubular cells and inflammatory profile.Analytical cellular pathology (Amsterdam) · 2015Article
- Prevalence of persistent microalbuminuria and associated factors among HIV infected children attending a Tertiary Hospital in Northern Tanzania: a cross sectional, analytical study.The Pan African medical journal · 2015Article
- HIV and chronic kidney disease.Clinical nephrology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-infected patients suffer several renal syndromes, which can progress rapidly from renal insufficiency to end-stage renal disease. Histologically, HIV-induced nephropathy is characterized by prominent tubulopathy with apoptosis of tubular cells. Clinical and experimental evidence suggests that renal injury may be directly related to virus infection. Although HIV-1 is a polytropic and not solely lymphotropic pathogen, the susceptibility of renal cells to HIV-1 remains to be determined. This paper demonstrates in vitro the permissiveness of proximal tubular epithelial cells (PTEC) to HIV-1 and describes the effects of PTEC infection to explain the pathogenesis of tubular damage in vivo. The results indicate that PTEC express HIV-specific receptor and coreceptors and sustain virus replication. We observed that HIV-1 infection causes the death of tubular cells by triggering an apoptotic pathway involving caspase activation. Fas upregulation but not Fas ligand expression was found in the infected PTEC. However, after HIV-1 infection, tubular cells became susceptible to apoptosis induced through Fas stimulation. Caspase inhibition prevented the death of the infected PTEC in spite of persistent viral replication. These findings may explain the prominent histopathology of HIV-associated nephropathy and demonstrate that the apoptosis of nonlymphoid cells can be directly induced by HIV-1.
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