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  3. Aortic Segments-depending Hypertensive Remodeling Is Driven By Mitochondrial Fusion Dysfunction.
  1. Home
  3. Aortic Segments-depending Hypertensive Remodeling Is Driven By Mitochondrial Fusion Dysfunction.

Related Experiment Video

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
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Published on: November 14, 2025

Aortic Segments-Depending Hypertensive Remodeling Is Driven by Mitochondrial Fusion Dysfunction.

Alexis Richard1, Alicia Baptista Vicente1, Clara Gourhand1

  • 1Univ Angers, INSERM, CNRS, MITOVASC, CARME Team, SFR ICAT, Angers, France.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 22, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

OPA1 deficiency worsens hypertension-induced aortic remodeling, particularly in the suprarenal abdominal aorta (SRAA). This highlights OPA1

Keywords:
Opa1 haploinsufficiencyaortic remodelinghypertensionmitochondrial dysfunctionsegmental vascular vulnerability

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10:21

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Published on: June 14, 2016

Area of Science:

  • Vascular Biology
  • Mitochondrial Biology
  • Hypertension Research

Background:

  • OPA1 is crucial for mitochondrial dynamics and homeostasis.
  • Hypertension causes significant aortic remodeling.
  • Segment-specific vulnerability in aortic disease is poorly understood.

Purpose of the Study:

  • To investigate the role of OPA1 in hypertension-induced aortic remodeling.
  • To determine if OPA1 deficiency causes segment-specific effects on the aorta.
  • To elucidate the molecular mechanisms underlying OPA1's protective function.

Main Methods:

  • Utilized Opa1+/- mice subjected to severe hypertension.
  • Analyzed aortic segments (SRAA and DTA) for mitochondrial function, apoptosis, and inflammation.
  • Employed morphometric analysis and in vivo ultrasound imaging.

    • Main Results:

    • OPA1 haploinsufficiency exacerbated aortic remodeling in a segment-specific manner (SRAA > DTA).
    • Hypertension activated mitochondrial fission and mitophagy markers in the SRAA, with compensatory upregulation of respiratory chain complexes.
    • Increased apoptosis and M1 macrophage infiltration were observed in the SRAA of hypertensive Opa1+/- mice.

    Conclusions:

    • OPA1 plays a critical protective role in the aortic wall against hypertensive stress.
    • The suprarenal abdominal aorta exhibits greater vulnerability to OPA1 deficiency under hypertension.
    • Findings suggest OPA1's region-specific function opens new therapeutic avenues for hypertension and aortic remodeling.