What question did this study set out to answer?

Investigate how HIV infection and antiretroviral therapy (ART) affect cardiomyocytes and contribute to cardiac dysfunction.

January 10, 2026Communications Medicine0 citationsOpen Access

Molecular insights in HIV-associated cardiac dysfunction

MVMaría Valero-MuñozBoston University ESEng Leng Saw DPDavid R. PimentelHeart Failure & Transplant

Key Result

Untreated HIV serum exposure results in dysregulated molecular pathways in cardiomyocytes, contributing to diastolic dysfunction and HFpEF in PLWH.

Key Points

Investigate how HIV infection and antiretroviral therapy (ART) affect cardiomyocytes and contribute to cardiac dysfunction.
Analyzed cardiomyocytes from patients with untreated HIV and those on ART.
Followed patients longitudinally to assess changes in cardiac function.
Compared molecular pathways in cardiomyocytes exposed to HIV serum versus ART-treated serum.
Dysregulated molecular pathways identified in cardiomyocytes exposed to untreated HIV serum.
ART treatment modified the cardiomyocyte phenotype.
Both HIV infection and ART contribute to diastolic dysfunction and HFpEF.

Structured PICO

Does in vitro exposure to serum from ART-treated PLWH alter cardiomyocyte apoptosis, calcium handling, and remodeling pathways compared to serum from ART-naïve PLWH?

Population

Adult rat ventricular cardiomyocytes (ARVMs) treated with serum from 10 persons living with HIV (PLWH) (100% male, mean age 32 ± 10 years, normotensive, no CAD) and 10 HIV-negative controls (70% male, mean age 52 ± 7 years).

Intervention

24-hour in vitro exposure to serum from PLWH after 6 months of combination antiretroviral therapy (elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate).

Comparator

24-hour in vitro exposure to serum from the same PLWH before ART initiation (ART-naïve) and serum from HIV-negative controls.

Outcome

Transcriptomic changes (RNA sequencing), apoptosis (TUNEL assay), cardiomyocyte size, calcium handling protein expression (SERCA2, PLB), and extracellular matrix remodeling markers.surrogate

Exposure to serum from ART-naïve PLWH increases cardiomyocyte apoptosis, whereas serum from ART-treated PLWH alters calcium handling and profibrotic pathways, suggesting complementary roles in HIV-associated HFpEF.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

These findings demonstrate dysregulated molecular pathways in cardiomyocytes following exposure to untreated HIV serum versus ART-treated HIV serum from patients followed longitudinally. Altogether, these data suggest that HIV infection and ART contribute to changes seen in the cardiomyocyte phenotype and play complementary roles in the pathogenesis of diastolic dysfunction and HFpEF in PLWH.

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