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Abnormal Proliferation

Abnormal Proliferation

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 daughter...

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

Separation of Sister Chromatids

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...

Mitogens and the Cell Cycle

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

Anaphase Promoting Complex

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

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Updated: May 10, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

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Podocyte loss involves MDM2-driven mitotic catastrophe.

Shrikant R Mulay¹, Dana Thomasova, Mi Ryu

¹Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universität, München, Germany.

The Journal of Pathology

|June 11, 2013

Summary

Blocking murine double minute (MDM)-2 unexpectedly reduced kidney injury markers by preventing podocyte mitotic catastrophe, a novel pathway of cell loss. MDM2 blockade offers a potential therapeutic strategy for progressive kidney disease.

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Last Updated: May 10, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

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Area of Science:

Nephrology
Molecular Biology
Cell Biology

Background:

Podocyte loss contributes to progressive kidney disease.
The mechanisms of podocyte death, including apoptosis and inflammatory forms, are not fully understood.
Murine double minute (MDM)-2 is implicated in regulating apoptosis and inflammation.

Purpose of the Study:

To investigate the role of MDM2 in podocyte death during glomerular injury.
To explore the potential of MDM2 blockade as a therapeutic strategy for kidney disease.

Main Methods:

Targeting MDM2 in mouse models of adriamycin-induced nephropathy.
In vitro studies using cultured podocytes exposed to adriamycin.
Analysis of human renal biopsies for features of podocyte mitotic catastrophe.

Main Results:

MDM2 blockade unexpectedly reduced kidney injury markers, inflammation, and podocyte loss in vivo.
In vitro, MDM2 blockade induced G2/M arrest in podocytes, preventing mitotic catastrophe.
Podocyte mitotic catastrophe was observed in human proteinuric kidney diseases.

Conclusions:

MDM2-mediated mitotic catastrophe is a novel mechanism of podocyte loss in kidney disease.
MDM2 blockade may represent a new therapeutic approach to prevent kidney inflammation and fibrosis.