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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.
Regulation of Stroke Volume01:27

Regulation of Stroke Volume

The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...

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Updated: May 8, 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

Caspase-3 modulates regenerative response after stroke.

Wenying Fan1, Yiqin Dai, Haochen Xu

  • 1State Key Laboratory of Medical Neurobiology, Shanghai Medical College and Institutes of Brain Science, Fudan University, Shanghai, People's Republic of China.

Stem Cells (Dayton, Ohio)
|August 14, 2013
PubMed
Summary
This summary is machine-generated.

Targeting caspase-3 promotes brain repair after stroke. Inhibiting caspase-3 boosts neurogenesis and functional recovery by enhancing neuronal precursor cell proliferation and migration.

Keywords:
Caspase-3NeurogenesisNeuronal precursor cellsStrokeStroke recovery

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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

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Last Updated: May 8, 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

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
11:32

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Cell Biology

Background:

  • Stroke is a major cause of disability with limited recovery therapies.
  • The adult brain's capacity for neurogenesis offers potential for stroke repair.
  • Mechanisms of stroke-induced neurogenesis remain largely unknown.

Purpose of the Study:

  • Investigate the role of caspase-3 in stroke-induced neurogenesis.
  • Determine if caspase-3 influences neuronal precursor cell (NPC) behavior post-stroke.
  • Explore caspase-3 inhibition as a therapeutic strategy for stroke recovery.

Main Methods:

  • Assessed cleaved caspase-3 levels in NPCs from SVZ and dentate gyrus post-stroke.
  • Examined caspase-3's effect on NPC self-renewal and proliferation in vitro.
  • Investigated caspase-3's impact on Akt phosphorylation in NPCs.
  • Utilized peptide inhibitors to block caspase-3 activity in vivo and in vitro.

Main Results:

  • Cleaved caspase-3 increased in NPCs during stroke recovery without inducing apoptosis.
  • Caspase-3 limited NPC self-renewal and proliferation by reducing Akt phosphorylation.
  • Inhibition of caspase-3 enhanced NPC proliferation and migration.
  • Caspase-3 inhibition led to increased neuronal regeneration and functional recovery post-stroke.

Conclusions:

  • Identified a novel caspase-3-dependent mechanism limiting endogenous neurogenesis after stroke.
  • Caspase-3 negatively regulates NPC proliferation and migration.
  • Targeting caspase-3 presents a promising therapeutic avenue for enhancing stroke recovery through neurogenesis.