Autophagy in peritoneal fibrosis

Front Physiol. 2023 May 15:14:1187207. doi: 10.3389/fphys.2023.1187207. eCollection 2023.


Peritoneal dialysis (PD) is a widely accepted renal replacement therapy for patients with end-stage renal disease (ESRD). Morphological and functional changes occur in the peritoneal membranes (PMs) of patients undergoing long-term PD. Peritoneal fibrosis (PF) is a common PD-related complication that ultimately leads to PM injury and peritoneal ultrafiltration failure. Autophagy is a cellular process of "self-eating" wherein damaged organelles, protein aggregates, and pathogenic microbes are degraded to maintain intracellular environment homeostasis and cell survival. Growing evidence shows that autophagy is involved in fibrosis progression, including renal fibrosis and hepatic fibrosis, in various organs. Multiple risk factors, including high-glucose peritoneal dialysis solution (HGPDS), stimulate the activation of autophagy, which participates in PF progression, in human peritoneal mesothelial cells (HPMCs). Nevertheless, the underlying roles and mechanisms of autophagy in PF progression remain unclear. In this review, we discuss the key roles and potential mechanisms of autophagy in PF to offer novel perspectives on future therapy strategies for PF and their limitations.

Keywords: autophagy; human peritoneal mesothelial cells; peritoneal dialysis; peritoneal dialysis-related peritonitis; peritoneal fibrosis.

Publication types

  • Review

Grants and funding

This work was supported by the Funds for the National Natural Science Foundation of China (grant numbers 81700627, 81670654, and 81974095), National Clinical Key Specialty Construction Project (Institute of Nephrology, Affiliated Hospital of Guangdong Medical University), Science and Technology Innovation Strategy of Guangdong Province (grant numbers 2019A1515010678 and 2018A030313231), Science and Technology Planning Project of Zhanjiang City (grant numbers 2021A05067 and 2021A05083), and Science Foundation of Guangdong Medical University (grant number GDMUM2020009).