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Caveolin-1 levels associated with coronary artery disease in Chinese participants: a retrospective cohort study

Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine

Frontiers in Cardiovascular MedicineLast synced 8/23/2026Status: syncedPMID: 42630195 pmidDOI: 10.3389/fcvm.2026.1790930

Background Coronary artery disease (CAD) remains a leading cause of mortality globally, yet approximately 30% of CAD risk remains unexplained by conventional factors. Caveolin-1 (Cav-1) regulates endothelial function through inhibiting endothelial nitric oxide synthase and promoting LDL transcytosis. While genome-wide association studies linked CAV1 variants to CAD risk (OR 1.19–1.23), whether circulating Cav-1 serves as a clinical biomarker for CAD risk stratification remains unknown. Methods This retrospective cohort study enrolled 160 participants (105 CAD patients, 55 controls) who underwent coronary angiography at Shanxi Provincial People's Hospital, China, from September 2024 to February 2025. CAD was defined as ≥50% stenosis in major coronary arteries. Serum Cav-1 levels were measured using ELISA. Multivariable logistic regression models adjusted for age, sex, lipids, and biomarkers evaluated Cav-1's independent association with CAD. Restricted cubic spline (RCS) analysis assessed dose-response relationships, and receiver operating characteristic (ROC) curves evaluated discriminative performance. Results CAD patients exhibited significantly lower Cav-1 levels than controls (7.0 ± 2.7 vs. 8.5 ± 2.7 ng/mL,= 0.001). After full adjustment, each 1 ng/mL increase in Cav-1 conferred 18% CAD risk reduction (OR 0.82, 95% CI 0.68–0.98,= 0.031). Participants in the highest Cav-1 quartile demonstrated 80% lower risk vs. the lowest quartile (OR 0.20, 95% CI 0.05–0.84,= 0.028;for tr

Abstract

Background Coronary artery disease (CAD) remains a leading cause of mortality globally, yet approximately 30% of CAD risk remains unexplained by conventional factors. Caveolin-1 (Cav-1) regulates endothelial function through inhibiting endothelial nitric oxide synthase and promoting LDL transcytosis. While genome-wide association studies linked CAV1 variants to CAD risk (OR 1.19–1.23), whether circulating Cav-1 serves as a clinical biomarker for CAD risk stratification remains unknown. Methods This retrospective cohort study enrolled 160 participants (105 CAD patients, 55 controls) who underwent coronary angiography at Shanxi Provincial People's Hospital, China, from September 2024 to February 2025. CAD was defined as ≥50% stenosis in major coronary arteries. Serum Cav-1 levels were measured using ELISA. Multivariable logistic regression models adjusted for age, sex, lipids, and biomarkers evaluated Cav-1's independent association with CAD. Restricted cubic spline (RCS) analysis assessed dose-response relationships, and receiver operating characteristic (ROC) curves evaluated discriminative performance. Results CAD patients exhibited significantly lower Cav-1 levels than controls (7.0 ± 2.7 vs. 8.5 ± 2.7 ng/mL,= 0.001). After full adjustment, each 1 ng/mL increase in Cav-1 conferred 18% CAD risk reduction (OR 0.82, 95% CI 0.68–0.98,= 0.031). Participants in the highest Cav-1 quartile demonstrated 80% lower risk vs. the lowest quartile (OR 0.20, 95% CI 0.05–0.84,= 0.028;for trend <0.01). RCS analysis revealed a consistent linear inverse relationship (for nonlinearity = 0.812). Combining Cav-1 with albumin significantly enhanced discrimination (AUC 88.4%, 95% CI 83.3–93.5), approaching the full multivariable model performance (AUC 89.8%). Conclusions Circulating Cav-1 demonstrates an independent, linear inverse association with CAD risk in Chinese adults. Combined with albumin, Cav-1 achieves robust discriminative performance, suggesting potential utility for refined risk stratification beyond traditional risk factors.

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