Metabolic reprogramming of peritoneal mesothelial cells in peritoneal dialysis–associated fibrosis: therapeutic targets and strategies DOI Creative Commons
Fang Yu, Jia Chen, Xiaoyue Wang

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 27, 2025

Peritoneal dialysis (PD) is considered a life-saving treatment for end-stage renal disease. However, prolonged PD use can lead to the development of peritoneal fibrosis (PF), diminishing its efficacy. mesothelial cells (PMCs) are key initiators PF when they become damaged. Exposure high glucose‑based fluids (PDFs) contributes by directly affecting highly metabolically active PMCs. Recent research indicates that PMCs undergo metabolic reprogramming exposed high-glucose PDFs, including enhanced glycolysis, impaired oxidative phosphorylation, abnormal lipid metabolism, and mitochondrial dysfunction. Although this transition temporarily compensates cellular damage maintains energy levels, long-term impact on tissue concerning. Multiple studies have identified close association between shift in metabolism PF, may promote progression through various molecular mechanisms. This review explores recent findings regarding role mechanism PMC progression. Moreover, it provides summary potential therapeutic strategies aimed at processes, glucose function. The establishes targeting be novel strategy preventing treating PD-associated fibrosis. Overview associated with implications. Under physiological conditions, primarily produce ATP OXPHOS FAO maintain functions. High-glucose PDFs induce PMCs, characterized increased polyol pathway, PPP, inhibited OXPHOS, FAO, exocytosis deposition, These changes multiple pathways. Potential target absorption, restoration, fatty acid oxidation; phosphorylation; PD, dialysis, PDF, fluid; PMC, cell; pentose phosphate pathway.

Language: Английский

Metabolic reprogramming of peritoneal mesothelial cells in peritoneal dialysis–associated fibrosis: therapeutic targets and strategies DOI Creative Commons
Fang Yu, Jia Chen, Xiaoyue Wang

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 27, 2025

Peritoneal dialysis (PD) is considered a life-saving treatment for end-stage renal disease. However, prolonged PD use can lead to the development of peritoneal fibrosis (PF), diminishing its efficacy. mesothelial cells (PMCs) are key initiators PF when they become damaged. Exposure high glucose‑based fluids (PDFs) contributes by directly affecting highly metabolically active PMCs. Recent research indicates that PMCs undergo metabolic reprogramming exposed high-glucose PDFs, including enhanced glycolysis, impaired oxidative phosphorylation, abnormal lipid metabolism, and mitochondrial dysfunction. Although this transition temporarily compensates cellular damage maintains energy levels, long-term impact on tissue concerning. Multiple studies have identified close association between shift in metabolism PF, may promote progression through various molecular mechanisms. This review explores recent findings regarding role mechanism PMC progression. Moreover, it provides summary potential therapeutic strategies aimed at processes, glucose function. The establishes targeting be novel strategy preventing treating PD-associated fibrosis. Overview associated with implications. Under physiological conditions, primarily produce ATP OXPHOS FAO maintain functions. High-glucose PDFs induce PMCs, characterized increased polyol pathway, PPP, inhibited OXPHOS, FAO, exocytosis deposition, These changes multiple pathways. Potential target absorption, restoration, fatty acid oxidation; phosphorylation; PD, dialysis, PDF, fluid; PMC, cell; pentose phosphate pathway.

Language: Английский

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