CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization.

ABSTRACT: Rationale: Sustained hypertension induces adverse cardiac remodeling. Platelet activation is instrumental in exacerbating inflammation by engaging with macrophages. C-C chemokine motif ligand 5 (CCL5) is contained within platelet α-granules, and released following platelet activation. This work delineated the specific contributions of CCL5 to platelet function, platelet-induced macrophage polarization, and hypertensive cardiac remodeling. Methods: CCL5 knockout (KO) mice infused with Angiotensin II (Ang II) were used to identify the role of CCL5 in vivo. CCL5 absence on platelet activation were evaluated on washed platelets. Two distinct models of platelet depletion and reconstitution were utilized to investigate the impact of platelets lacking CCL5. An in vitro

SUBMITTER: Lv S 

PROVIDER: S-EPMC12674933 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature