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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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Nucleophosmin Promotes Regulated Cell Death in Podocyte Injury.

Seiya Urae1, Zhiyong Wang1, Sudhir Kumar1

  • 1Department of Medicine, Section of Nephrology, Boston University Chobanian and Avedisian School of Medicine and Boston Medical Center, Boston, Massachusetts.

Kidney360
|September 16, 2025
PubMed
Summary
This summary is machine-generated.

Cytosolic nucleophosmin (NPM) accumulation drives podocyte injury in kidney disease. Inhibiting NPM/Bax interaction protects podocytes from stress-induced death, offering a potential therapeutic strategy for glomerulopathy.

Keywords:
CKDapoptosiscell deathchronic GNglomerulopathykidney biopsymitochondriapodocyte

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Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies
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Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • The mechanism of podocyte death in glomerulopathy remains unclear, hindering therapeutic development.
  • Cytosolic accumulation of nucleophosmin (NPM) is hypothesized to promote podocyte injury via Bax during glomerulopathy.

Purpose of the Study:

  • To investigate the role of cytosolic NPM accumulation in podocyte injury and death.
  • To explore NPM/Bax interaction as a therapeutic target for protecting podocytes.

Main Methods:

  • Quantified NPM in human podocytes and mouse/human kidney tissues under stress and disease conditions.
  • Assessed NPM/Bax complex formation, mitochondrial Bax translocation, and podocyte survival.
  • Manipulated NPM levels and tested therapeutic peptides targeting NPM/Bax interaction.

Main Results:

  • Cytosolic NPM accumulated in response to stressors, increasing NPM/Bax complex formation and mitochondrial Bax.
  • NPM suppression enhanced podocyte survival; NPM overexpression reduced it.
  • A peptide inhibiting NPM/Bax interaction improved podocyte survival.
  • Increased NPM and cytosolic NPM were observed in mouse models and human glomerulopathy.

Conclusions:

  • Cytosolic NPM translocation is linked to experimental and clinical podocyte injury.
  • NPM promotes regulated podocyte death following stress.
  • Targeting NPM/Bax interaction represents a promising therapeutic avenue for glomerular injury protection.