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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

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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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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Related Experiment Video

Updated: Apr 11, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
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PUMA-mediated mitochondrial apoptotic disruption by hypoxic postconditioning.

YuZhen Li1, Qi Guo, XiuHua Liu

  • 1Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, 100853, China, yuzlif96@163.com.

Apoptosis : an International Journal on Programmed Cell Death
|June 6, 2015
PubMed
Summary

Hypoxic postconditioning protects heart cells from injury by reducing PUMA protein levels, thereby inhibiting the mitochondrial apoptosis pathway. This finding reveals a key mechanism for postconditioning

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Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Mitochondrial Function

Background:

  • Ischemia-reperfusion (I/R) injury causes cardiomyocyte apoptosis, contributing to heart damage.
  • Mitochondria play a crucial role in the apoptotic process during I/R injury.
  • p53 upregulated modulator of apoptosis (PUMA) is implicated in lethal I/R injury.

Purpose of the Study:

  • To investigate whether hypoxic postconditioning inhibits mitochondrial pathway-mediated cardiomyocyte apoptosis by regulating PUMA expression.
  • To elucidate the role of PUMA in the cardioprotective effects of postconditioning.

Main Methods:

  • Neonatal rat cardiomyocytes were subjected to hypoxia and reoxygenation.
  • Postconditioning was induced using cycles of hypoxia and reoxygenation.
  • Levels of PUMA mRNA and protein were measured.
  • Mitochondrial membrane potential, cytochrome c release, and caspase-3 activation were assessed.
  • PUMA was overexpressed to evaluate its impact under postconditioning.

Main Results:

  • Hypoxic postconditioning significantly reduced PUMA mRNA and protein levels.
  • Postconditioning attenuated the loss of mitochondrial membrane potential, cytochrome c release, and caspase-3 activation.
  • Overexpression of PUMA counteracted the protective effects of postconditioning, increasing apoptosis and mitochondrial dysfunction.

Conclusions:

  • Reduction of PUMA expression is a key mechanism underlying the cardioprotective effects of postconditioning.
  • Postconditioning disrupts the mitochondrial apoptotic pathway by modulating PUMA.
  • Targeting PUMA may offer a therapeutic strategy for mitigating I/R injury in the heart.