ArticleCardiovascular diabetology2025
Activated protein C ameliorates diabetes-induced atherosclerosis by sustaining macrophage efferocytosis.
Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- [Research advances on the targeted programmed cell death regulatory network for treatment of refractory diabetic wounds].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2026Review
- Correction: Activated protein C ameliorates diabetes-induced atherosclerosis by sustaining macrophage efferocytosis.Cardiovascular diabetology · 2026Article
- Protease-activated receptor 1 in diabetes and its chronic complications: signaling mechanisms and emerging therapeutic advances.Frontiers in pharmacology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Macrophage efferocytosis, essential for the resolution of inflammation and plaque stability in atherosclerosis, is impaired in diabetes. Thrombomodulin (TM) and endothelial protein C receptor (EPCR), key mediators of protein C activation (PC), have vasculoprotective and anti-inflammatory roles, yet their involvement in macrophage efferocytosis in diabetes-induced atherosclerosis remains unclear. Here, we demonstrate that expression of EPCR was reduced in atherosclerotic lesions of diabetic patients compared to non-diabetic controls. In parallel, efferocytosis was impaired in atherosclerotic lesions and in monocytes derived macrophages of diabetic patients. In vitro, treatment with activated PC (aPC) or its cytoprotective selective variant (3K3A-aPC) restored high glucose-impaired macrophage efferocytosis. Mechanistic studies revealed that aPC restored efferocytosis through Arginase-1 and modulation of Rac1-ATF6 signaling. Additionally, macrophage protease-activated receptor 1 (PAR1) was identified as the key receptor mediating aPC's effects on efferocytosis. Mimicking biased PAR-1 signaling via parmodulin-2 reverses glucose impaired efferocytosis. In vivo, aPC treatment of diabetic ApoE
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