AIDS. 2026 Mar 31. doi: 10.1097/QAD.0000000000004507. Online ahead of print.
ABSTRACT
OBJECTIVE: To determine whether HIV-1 gp120 impairs cardiomyocyte bioenergetics.
DESIGN/METHODS: We exposed neonatal rat ventricular myocytes to gp120 and measured mitochondrial respiration, gene expression, and metabolites.
RESULTS: gp120 reduced maximal and spare respiratory capacity (p < 0.0001), induced PTBP1 upregulation with PKM1-to-PKM2 switching, and increased lactate production.
CONCLUSIONS: gp120 causes cardiac metabolic reprogramming and mitochondrial dysfunction. The PTBP1-PKM2 axis represents a potential therapeutic target for HIV-associated cardiovascular disease.
PMID:41921077 | DOI:10.1097/QAD.0000000000004507