The Emerging Role of Interleukin-32 in HIV-Associated Cardiovascular Comorbidities: A Mini Review
With the widespread use of antiretroviral therapy (ART), the life expectancy of people living with HIV (PLWH) has significantly improved. However, the incidence of cardiovascular disease (CVD) in this population has progressively increased. PLWH exhibit a significantly higher risk of cardiovascular diseases compared to the general population. Consequently, CVD has become one of the leading contributors to mortality not related to AIDS. The pathogenesis may involve several factors: HIV-related proteins exacerbating endothelial injury and inflammation; immune activation and chronic inflammation; adverse effects of ART; and traditional cardiovascular risk factors. Although multiple inflammatory cytokines are implicated in HIV-associated CVD, interleukin-32 (IL-32) stands out due to its distinctive multifunctional properties. Compared with other cytokines, Interleukin-32 (IL-32), a multifunctional pro-inflammatory cytokine, plays key roles in inducing the release of inflammatory cytokines, promoting endothelial dysfunction, and driving monocyte migration. IL-32 is closely associated with the development of HIV-associated CVD and shows potential as a novel biomarker and therapeutic target. This review aims to summarize recent advances in understanding the role of IL-32 in HIV-associated CVD. It also provides new insights for the diagnosis and treatment of CVD in PLWH.
Authors
- Mingjian Ni (ORCID: https://orcid.org/0009-0006-0275-7914)
- Lina Chen
- Yitong Ma
- Jie Zhou
Institutions
- Xinjiang Medical University (CN)
- First Affiliated Hospital of Xinjiang Medical University (CN)
- Xinjiang Uygur Autonomous Region Disease Prevention and Control Center (CN)
- People's Hospital of Xinjiang Uygur Autonomous Region (CN)
Publication Details
- Journal
- International Journal of General Medicine
- Published
- 2026-02-01
- DOI
- https://doi.org/10.2147/ijgm.s579526
- Primary Topic
- Cytokine Signaling Pathways and Interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00