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The selected pathophysiological aspects of PPARs activation.
B Kieć-Wilk1, A Dembińska-Kieć, A Olszanecka
1Department of Clinical Biochemistry, Medical College Jagiellonian University, Kopernika 15a, 30-504 Krakow, Poland. mbkiec@cyf-kr.edu.pl
Summary
Peroxisome proliferator activated receptors (PPARs) regulate metabolism and offer cardiovascular protection. However, PPARs activation may cause lipotoxicity in cardiomyocytes, contributing to cardiac hypertrophy in metabolic diseases.
Area of Science:
- Cardiovascular Biology
- Metabolic Regulation
- Molecular Endocrinology
Background:
- Peroxisome proliferator activated receptors (PPARs) are nuclear transcription factors regulating glucose and lipid metabolism.
- Three PPAR isoforms (alpha, beta/delta, gamma) exist, with diverse tissue distribution and functions.
- PPARs exhibit anti-atherogenic, anti-inflammatory, and anti-hypertensive properties, including cardioprotection in hypertension-induced cardiac hypertrophy.
Purpose of the Study:
- To review the dual role of PPARs activation in cardiac pathophysiology.
- To explore the potential unfavorable effects of PPARs on lipid metabolism in cardiomyocytes.
- To discuss the implications of PPARs activation in conditions like diabetes, metabolic syndrome, and obesity.
Main Methods:
- Literature review of experimental reports and hypotheses.
- Analysis of existing evidence on PPARs function and dysfunction.
- Synthesis of pathophysiological aspects of PPARs activation in cardiac hypertrophy.
Main Results:
- PPARs activation demonstrates cardioprotective effects in hypertension-induced cardiac hypertrophy.
- Emerging evidence suggests PPARs activation can induce lipotoxicity in cardiomyocytes.
- This lipotoxicity may contribute to pathological cardiac hypertrophy in metabolic diseases.
Conclusions:
- PPARs possess a complex role in cardiac health, with both beneficial and detrimental effects.
- Understanding the balance of PPARs activation is crucial for managing metabolic and cardiovascular diseases.
- Further research is needed to elucidate the precise mechanisms of PPARs-induced lipotoxicity and its clinical relevance.