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Updated: Jun 18, 2026
07:29
Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Metabolic and redox pathway dysregulation in HIV-associated coronary endothelial dysfunction
Kshipra S Keole1, Syed Bukhari1, Anum Minhas1
1Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Summary
People with HIV face higher cardiovascular risk due to coronary endothelial dysfunction. This dysfunction is linked to metabolic and redox pathway imbalances, suggesting new therapeutic targets for HIV patients.
Area of Science:
- Cardiovascular Research
- Proteomics
- HIV Medicine
Background:
- People with HIV (PWH) on antiretroviral therapy have elevated cardiovascular disease (CVD) risk despite viral suppression.
- Underlying biological mechanisms for this residual CVD risk remain unclear.
- Coronary endothelial dysfunction is a key contributor to CVD.
Purpose of the Study:
- To investigate the association between coronary endothelial dysfunction and circulating proteomic signatures in virally suppressed PWH.
- To explore potential mechanisms involving metabolic and redox pathway dysregulation.
Main Methods:
- Prospective observational study integrating stress cardiovascular magnetic resonance imaging (CMR) and high-throughput serum proteomics (SomaScan 7K).
- Quantified coronary endothelial function via CMR during isometric handgrip exercise.
- Analyzed differential protein expression using linear modeling.
Main Results:
- Coronary endothelial dysfunction was significantly more prevalent in PWH (67%) than controls (10%).
- Pathway enrichment analysis revealed significant dysregulation in glutathione-dependent detoxification, oxidative metabolism, and fatty acid β-oxidation pathways.
- No distinct baseline clinical or proteomic profile fully explained the difference between PWH and controls.
Conclusions:
- Coronary endothelial dysfunction in virally suppressed PWH is associated with metabolic and redox imbalance.
- Glutathione and fatty acid oxidation pathways are potential therapeutic targets to reduce residual CVD risk in PWH.
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