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Autophagy and the Peroxisome Proliferator-Activated Receptor Signaling Pathway: A Molecular Ballet in Lipid Metabolism and Homeostasis Publisher



Kiani P1 ; Khodadadi ES2 ; Nikdasti A12 ; Yarahmadi S3 ; Gheibi M4 ; Yousefi Z5 ; Ehtiati S6 ; Yahyazadeh S7 ; Shafiee SM8 ; Taghizadeh M9 ; Igder S10 ; Khatami SH6 ; Karima S11 ; Vakili O1 Show All Authors
Authors
  1. Kiani P1
  2. Khodadadi ES2
  3. Nikdasti A12
  4. Yarahmadi S3
  5. Gheibi M4
  6. Yousefi Z5
  7. Ehtiati S6
  8. Yahyazadeh S7
  9. Shafiee SM8
  10. Taghizadeh M9
  11. Igder S10
  12. Khatami SH6
  13. Karima S11
  14. Vakili O1
  15. Pourfarzam M1
Show Affiliations
Authors Affiliations
  1. 1. Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Pharmaceutical and Pharmacological Sciences, University of Padova, 35122, Padova, Italy
  3. 3. Nutritional Health Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran
  4. 4. Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
  5. 5. Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  6. 6. Student Research Committee, Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  7. 7. Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  8. 8. Autophagy Research Center, Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  9. 9. Department of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  10. 10. Department of Clinical Biochemistry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  11. 11. Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran
  12. 12. Department of Comparative Biomedicine and Food Science, University of Padova, Viale dell’Universita 16, 35020, Legnaro, Padova, Italy

Source: Molecular and Cellular Biochemistry Published:2025


Abstract

Lipids, which are indispensable for cellular architecture and energy storage, predominantly consist of triglycerides (TGs), phospholipids, cholesterol, and their derivatives. These hydrophobic entities are housed within dynamic lipid droplets (LDs), which expand and contract in response to nutrient availability. Historically perceived as a cellular waste disposal mechanism, autophagy has now been recognized as a crucial regulator of metabolism. Within this framework, lipophagy, the selective degradation of LDs, plays a fundamental role in maintaining lipid homeostasis. Dysregulated lipid metabolism and autophagy are frequently associated with metabolic disorders such as obesity and atherosclerosis. In this context, peroxisome proliferator-activated receptors (PPARs), particularly PPAR-γ, serve as intracellular lipid sensors and master regulators of gene expression. Their regulatory influence extends to both autophagy and lipid metabolism, indicating a complex interplay between these processes. This review explores the hypothesis that PPARs may directly modulate autophagy within the realm of lipid metabolism, thereby contributing to the pathogenesis of metabolic diseases. By elucidating the underlying molecular mechanisms, we aim to provide a comprehensive understanding of the intricate regulatory network that connects PPARs, autophagy, and lipid homeostasis. The crosstalk between PPARs and other signaling pathways underscores the complexity of their regulatory functions and the potential for therapeutic interventions targeting these pathways. The intricate relationships among PPARs, autophagy, and lipid metabolism represent a pivotal area of research with significant implications for understanding and treating metabolic disorders. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.
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