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Complement induces podocyte pyroptosis in membranous nephropathy by mediating mitochondrial dysfunction.

Hui Wang1, Daoyuan Lv1, Song Jiang1

  • 1National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu, China.

Cell Death & Disease
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Pyroptosis, a programmed cell death, drives podocyte injury in membranous nephropathy (MN) by activating complement. Inhibiting pyroptosis or reactive oxygen species (ROS) offers potential therapeutic strategies for MN.

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Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Membranous nephropathy (MN) pathogenesis involves podocyte damage from in situ complement activation.
  • The precise molecular mechanisms underlying podocyte injury in MN remain incompletely understood.
  • Pyroptosis, a pro-inflammatory programmed cell death, is implicated in tissue injury but its role in MN is unclear.

Purpose of the Study:

  • To investigate the role of pyroptosis in podocyte injury during membranous nephropathy (MN).
  • To elucidate the molecular mechanisms linking complement activation, pyroptosis, and podocyte damage in MN.
  • To evaluate the therapeutic potential of targeting pyroptosis in MN.

Main Methods:

  • Observed pyroptosis in kidney biopsies from MN patients.
  • Utilized in vitro podocyte cultures stimulated with complement to assess pyroptosis induction and inhibition.
  • Investigated the role of mitochondrial depolarization and reactive oxygen species (ROS) in complement-induced pyroptosis.
  • Employed passive Heymann nephritis (PHN) rat models and pyroptosis inhibitors for in vivo validation.

Main Results:

  • Pyroptosis was identified in the kidneys of MN patients.
  • Complement stimulation triggered pyroptosis in podocytes, leading to cell damage; inhibition reversed these effects.
  • Complement-induced pyroptosis involved mitochondrial depolarization and ROS production; ROS inhibition partially reversed pyroptosis.
  • Inhibition of pyroptosis ameliorated kidney damage in PHN rat models.

Conclusions:

  • Pyroptosis plays a critical role in complement-mediated podocyte injury in membranous nephropathy.
  • Mitochondrial dysfunction and ROS production are key mechanisms in complement-induced pyroptosis in podocytes.
  • Targeting pyroptosis presents a promising novel therapeutic strategy for treating MN.