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[PPARs and fibrosis].

Masahiko Kurabayashi¹

¹Department of Medicine and Biological Science, Gunma University Graduate School of Medicine.

Nihon Rinsho. Japanese Journal of Clinical Medicine

|April 15, 2005

Summary

Inflammation contributes to fibrosis, particularly in the heart. PPARs may offer a therapeutic strategy by targeting inflammation and reactive oxygen species production linked to Angiotensin II.

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Area of Science:

Cardiovascular Research
Molecular Biology
Pharmacology

Background:

Inflammation is intrinsically linked to fibrotic processes, notably in cardiac remodeling associated with hypertension and ischemia.
Angiotensin II (AngII) promotes fibroblast growth and collagen synthesis, key factors in cardiac remodeling.
AngII stimulates reactive oxygen species (ROS) production via NADPH oxidase, contributing to tissue injury in various organs.

Purpose of the Study:

To explore the role of Angiotensin II in inflammation-driven cardiac fibrosis.
To investigate the potential of Peroxisome proliferator-activated receptors (PPARs) as therapeutic targets for cardiac and perivascular fibrosis.

Main Methods:

Review of published studies on Angiotensin II, ROS, NADPH oxidase, and PPARs.
Analysis of the molecular mechanisms linking AngII, ROS, inflammation, and fibrosis.
Evaluation of PPARs' inhibitory effects on NADPH oxidase and NF-kappaB activation.

Main Results:

Angiotensin II enhances ROS production, contributing to tissue injury and fibrosis.
PPARgamma ligands have been shown to reduce NADPH oxidase activity.
PPARs inhibit inflammation by blocking NF-kappaB activation, a redox-sensitive transcription factor.

Conclusions:

PPARs represent promising therapeutic targets for mitigating cardiac and perivascular fibrosis.
Targeting PPARs may offer a strategy to counteract AngII-induced inflammation and ROS production, thereby reducing fibrotic remodeling.

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