Impaired lymphangiogenesis in pericoronary adipose tissue correlates with diabetes-aggravated coronary atherosclerosis

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Epicardial adipose tissue (EpAT), particularly pericoronary adipose tissue (PCAT), plays a crucial role in diabetes mellitus (DM)-aggravated coronary artery disease (CAD). Emerging evidence suggests that dysfunction of the arterial lymphatic network contributes to atherosclerosis progression. Our study aimed to investigate whether lymphatic vessel impairment in PCAT (a type of EpAT) is involved in DM-related CAD and to explore its underlying molecular mechanisms. Methods We prospectively enrolled patients undergoing heart valve surgery (control [CTRL] group) and coronary artery bypass grafting surgery (CAD group) between February 2024 and March 2025. EpAT volume (EpATv) and SYNTAX scores were assessed, and human PCAT samples were performed with pathological staining. Single-nucleus RNA sequencing (snRNA-seq) was employed to characterize intercellular communication between epicardial adipocytes and lymphatic endothelial cells (LECs). In vitro diabetic models of human adipocytes and LECs were established using palmitic acid (PA) and high concentration glucose (HG) to verify intercellular signaling. Results Of a total of 160 patients enrolled (113 males), 48 were controls and 112 were CAD patients (44 with DM). CAD patients, particularly those with DM, showed increased EpATv, adipocyte size, macrophage infiltration, and reduced lymphatic vessel density. Lymphatic vessel

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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