Impaired lymphangiogenesis in pericoronary adipose tissue correlates with diabetes-aggravated coronary atherosclerosis
Authors' conclusion
Our findings demonstrate that attenuated IGF1-IGF1R signaling between epicardial adipocytes and LECs may contribute to lymphatic impairment in PCAT, which is associated with CAD progression in DM. Our work may represent a novel potential therapeutic target for CAD patients with DM.
Study context
- Population
- Patients undergoing heart valve surgery or CABG surgery, February 2024–March 2025; 113 males; 44 coronary artery disease (CAD) patients with diabetes mellitus (DM)113 males
- Participants
- 160 patients
- Comparison
- CAD patients vs controls undergoing heart valve surgery
- CTRLn = 48reference
- CADn = 112
- Outcome
- Lymphatic vessel impairment in PCAT and underlying mechanisms
Methodological detailsprospective enrolment, single-nucleus RNA sequencing, in vitro diabetic models
- Prospective enrolment
- Single-nucleus RNA sequencing
- In vitro diabetic models
Main finding
As reported in the abstract
- CAD patients, particularly those with DM, showed increased epicardial adipose tissue (EpAT) volume, adipocyte size, macrophage infiltration, and reduced lymphatic vessel density
- Lymphatic vessel density inversely correlated with adipocyte size and CAD severity
- Single-nucleus RNA sequencing (snRNA-seq): significantly attenuated IGF1-IGF1R signaling between epicardial adipocytes and lymphatic endothelial cells (LECs) in pericoronary adipose tissue (PCAT) of CAD patients with DM
- Recombinant IGF1 enhanced LEC proliferation, migration and tube formation under diabetic conditions; IGF1R antagonist impeded these effects
Further findings
- CAD patients with DM had worse prognosis and higher readmission rates
Original publication
Impaired lymphangiogenesis in pericoronary adipose tissue correlates with diabetes-aggravated coronary atherosclerosis. Cardiovasc Diabetol. Published 24 January 2026. doi:10.
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