Inflammation-associated Lipidomic Signatures Prior to Carotid Artery Atherosclerosis in People Living With HIV
Authors' conclusion
Our findings underscore specific lipidomic-inflammatory networks that may underlie the heightened risk of atherosclerosis in HIV infection. The differential involvement of IL-18 suggests a central role of NLRP3 inflammasome activation in HIV-associated vascular inflammation. The observed alterations in lysophospholipid and short-chain fatty acyl metabolism warrant further mechanistic investigation as potential mediators of HIV-related atherogenesis.
Study context
- Population
- People living with HIV, Comparative HIV and Aging Research Cohort, Taizhou, China
- Participants
- 115 / 112 / 117
- Comparison
- HIV-positive incident subclinical carotid atherosclerosis (SCA) cases vs HIV-positive normal controls vs HIV-negative normal controls
- SCA casesn = 115
- HIV-positive normal controlsn = 112
- HIV-negative normal controlsn = 117reference
- Outcome
- Baseline lipidomic signatures (649 lipid species, 20 inflammatory markers)
- Follow-up
- Baseline
Methodological detailsUntargeted lipidomic profiling and inflammatory marker assessments at baseline and follow-up
- Untargeted lipidomic profiling and inflammatory marker assessments at baseline and follow-up
Main finding
As reported in the abstract
- Three distinct baseline lipidomic signatures: 1 upregulated in HIV infection, 1 downregulated, 1 upregulated in HIV-associated SCA
- 3
Observational data: associations, not effects.
Original publication
Inflammation-associated Lipidomic Signatures Prior to Carotid Artery Atherosclerosis in People Living With HIV. J Clin Endocrinol Metab. Published 9 June 2025. doi:10.
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