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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
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RhoA accelerates atherosclerosis progression by interacting with Hspa5.

Ruoyu Dong1, Can Cao2, Jikuan Li1

  • 1Department of Vascular Surgery, Hebei General Hospital, No.348, Heping West Road, Shijiazhuang, 050000, Hebei, China.

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|January 6, 2026
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Summary

RhoA protein promotes atherosclerosis (AS) by enhancing vascular smooth muscle cell migration and mitophagy. Targeting RhoA and its interaction with Hspa5 may offer new therapeutic strategies for AS treatment.

Keywords:
AtherosclerosisHspa5MitophagyRhoAVascular smooth muscle cells

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Biology

Background:

  • Atherosclerosis (AS) is a complex cardiovascular disease.
  • The precise regulatory mechanisms of RhoA in AS remain unclear.

Purpose of the Study:

  • To investigate the role and underlying mechanisms of RhoA in AS progression.
  • To explore the interaction between RhoA and Hspa5 in the context of AS.

Main Methods:

  • Established a high-fat diet-induced AS mouse model.
  • Utilized adeno-associated viruses for RhoA manipulation in vivo.
  • Analyzed oxidized low-density lipoprotein (ox-LDL) treated mouse aortic vascular smooth muscle cells (MOVAS) using various assays (cell counting kit-8, Transwell migration, electron microscopy, western blotting).
  • Investigated RhoA-Hspa5 interaction via bioinformatic analysis, co-immunoprecipitation, and immunofluorescence.

Main Results:

  • RhoA was significantly upregulated in AS mice and localized in the aortic smooth muscle layer.
  • RhoA inhibition suppressed MOVAS cell viability, migration, invasion, and mitophagy in vitro, and reduced AS plaque formation and inflammation in vivo.
  • Hspa5 was identified to interact with RhoA, with its expression positively correlated to RhoA levels.
  • Hspa5 overexpression reversed the inhibitory effects of RhoA silencing on cellular behaviors and AS progression.

Conclusions:

  • RhoA promotes AS by enhancing vascular smooth muscle cell migration, invasion, and mitophagy through interaction with Hspa5.
  • RhoA plays a critical role in exacerbating AS progression.
  • RhoA represents a potential therapeutic target for managing atherosclerosis.