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Peer-reviewedCC BYCells

Podocyte Metabolic Flexibility Under Stress Conditions: From Metabolic Adaptation to Maladaptive Responses.

  1. 1Laboratory of Metabolic and Molecular Biochemistry, Faculty of Medicine and Pharmacy, Research Institute for Health Sciences and Technology, University of Mons, 7000 Mons, Belgium.
  2. 2Laboratory of Human Biology and Toxicology, Faculty of Medicine and Pharmacy, Research Institute for Health Sciences and Technology, University of Mons, 7000 Mons, Belgium.
  3. 3French National Institute of Health and Medical Research (INSERM) CORAKID U155, Department of Nephrology, Assistance Publique-Hôpitaux de Paris (AP-HP), Tenon Hospital, Sorbonne University, 75020 Paris, France.

Abstract

Podocytes are essential for glomerular function by maintaining the integrity of the glomerular filtration barrier. As terminally differentiated, post-mitotic cells, they are highly vulnerable to injury, which represents a central event in the development of chronic kidney disease. Although podocytes have been extensively studied to elucidate their structure and function, their metabolism and the role of metabolic dysregulation in podocyte injury remain incompletely understood. This review summarizes current knowledge of podocyte metabolism and its responses to diverse stressors. We discuss the basal metabolic profile of podocytes, which remains a matter of debate in the literature, with a focus on mitochondrial function. We further examine how stress conditions such as gluco- and lipotoxicity, vasoactive stress, mechanical stress, and immune dysregulation induce metabolic adaptations that become maladaptive upon sustained exposure. Metabolic reprogramming and its consequences, including cytoskeletal disorganization, are reviewed alongside emerging therapeutic strategies aimed at restoring podocyte metabolic homeostasis. A better understanding of podocyte metabolic flexibility may provide innovative strategies to preserve podocyte integrity and prevent the progression of chronic kidney disease.

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BibTeX
@article{thirion2026podocyte,
  title = {{Podocyte Metabolic Flexibility Under Stress Conditions: From Metabolic Adaptation to Maladaptive Responses.}},
  author = {Marine Thirion and Emmanuel Esteve and Vanessa Tagliatti and Anne-Emilie Declèves},
  journal = {Cells},
  year = {2026},
  month = sep,
  doi = {10.3390/cells15191751},
  url = {https://europepmc.org/article/MED/42882449},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Podocyte Metabolic Flexibility Under Stress Conditions: From Metabolic Adaptation to Maladaptive Responses.
AU  - Marine Thirion
AU  - Emmanuel Esteve
AU  - Vanessa Tagliatti
AU  - Anne-Emilie Declèves
PY  - 2026
DA  - 2026/09/26
JO  - Cells
DO  - 10.3390/cells15191751
UR  - https://europepmc.org/article/MED/42882449
AB  - Podocytes are essential for glomerular function by maintaining the integrity of the glomerular filtration barrier. As terminally differentiated, post-mitotic cells, they are highly vulnerable to injury, which represents a central event in the development of chronic kidney disease. Although podocytes have been extensively studied to elucidate their structure and function, their metabolism and the role of metabolic dysregulation in podocyte injury remain incompletely understood. This review summarizes current knowledge of podocyte metabolism and its responses to diverse stressors. We discuss the basal metabolic profile of podocytes, which remains a matter of debate in the literature, with a focus on mitochondrial function. We further examine how stress conditions such as gluco- and lipotoxicity, vasoactive stress, mechanical stress, and immune dysregulation induce metabolic adaptations that become maladaptive upon sustained exposure. Metabolic reprogramming and its consequences, including cytoskeletal disorganization, are reviewed alongside emerging therapeutic strategies aimed at restoring podocyte metabolic homeostasis. A better understanding of podocyte metabolic flexibility may provide innovative strategies to preserve podocyte integrity and prevent the progression of chronic kidney disease.
SN  - 2073-4409
ER  -