Related Experiment Video

Updated: Jun 5, 2026

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction
08:41

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction

Published on: January 12, 2016

[Relationship between hypoxia-induced apoptosis and caspases-3 activation, intracellular calcium overload in

Zhou Zhou1, Xiao-hua Wang, Guang-xu Zhu

  • 1Department of Occupational Health, Third Military Medical University, Chongqing 400038, China.

Zhongguo Ying Yong Sheng Li Xue Za Zhi = Zhongguo Yingyong Shenglixue Zazhi = Chinese Journal of Applied Physiology
|December 21, 2010
PubMed

Insights

Hypoxia triggers cardiomyocyte apoptosis via Caspase-3 activation. Intracellular calcium overload plays a key role in this process, highlighting potential therapeutic targets.

Area of Science:

  • Cardiology
  • Cell Biology
  • Biochemistry

Context:

  • Hypoxia, a condition of oxygen deprivation, is a critical factor in cardiovascular diseases.
  • Understanding cellular mechanisms of injury during hypoxia is vital for developing treatments.
  • Cardiomyocytes are particularly vulnerable to hypoxic damage.

Purpose:

  • To investigate the impact of hypoxia on Caspase activation in cardiomyocytes.
  • To elucidate the role of intracellular calcium in hypoxia-induced Caspase activation and apoptosis.

Summary:

  • Hypoxia induces mitochondrion-dependent Caspase-3 activation, leading to cardiomyocyte apoptosis.
  • Mitochondrial cytochrome c release and Caspase-3 mRNA expression increase post-hypoxia.
  • Intracellular calcium overload precedes cytochrome c release and Caspase-3 activation.

Impact:

  • Findings reveal a critical pathway linking hypoxia, calcium signaling, and cardiomyocyte death.
  • Inhibiting Caspase-3 or chelating intracellular calcium demonstrates a protective effect against hypoxic injury.
  • This research provides insights into potential therapeutic strategies for hypoxic heart conditions.
Abstract

More Related Videos

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...