HIV-1 gp120 exposure associates with mitochondrial and PKM remodeling in cardiomyocytes

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.