HIV infection drives proinflammatory adipocyte differentiation in an in vitro model and reveals a new inflammatory pathway.
Freiberger RN., López CAM., Sviercz FA., Jarmoluk P., Palma MB., García MN.
Laboratory Study, published in Front Cell Infect Microbiol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Front Cell Infect Microbiol (2025)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40746960
- DOI
- 10.3389/fcimb.2025.1627963
Abstract (original English)
Adipose tissue regulates metabolic homeostasis and serves as a reservoir for mesenchymal stem cells (MSCs), which differentiate into osteoblasts and adipocytes, balancing bone and lipid metabolism. Bone loss and fat accumulation are common in individuals living with HIV, prompting us to investigate how R5- and X4-tropic HIV modulates adipocyte differentiation and tissue homeostasis using an in vitro model of MSC-derived adipogenesis. The study used an in vitro model of MSCs to examine how R5- and X4-tropic HIV strains affect adipocyte differentiation and function. Researchers assessed adipogenesis by analyzing lipid droplet formation, expression of adipogenic transcription factors (C/EBPα, C/EBPβ, PPAR-γ), lipogenic/lipolytic enzymes, SREBPs, cytokine secretion, and the effects of CXCR4 and CCR5 with specific inhibitors. HIV exposure influences adipogenesis, increasing lipid droplet size in a tropism dependent manner and upregulating key adipogenic factors such as C/EBPα, C/ EBPβ, and PPAR-γ. This process involves the regulation of lipogenic and lipolytic enzymes, lipid droplet-lysosome interactions, and potential lipid droplet mitochondria cross-talk to fuel lipid accumulation. Additionally, HIV modulates sterol regulatory element-binding proteins (SREBPs), which control fatty acid, triacylglycerol, and cholesterol synthesis. Notably, SREBP2 downregulation correlates with incr
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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