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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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...
Autophagic Cell Death01:18

Autophagic Cell Death

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Autophagy and Apoptosis
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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...

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Related Experiment Video

Updated: Jul 11, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Targeting cell death.

D J Hausenloy1, L Scorrano

  • 1The Hatter Cardiovascular Institute, University College London Hospital, London, UK.

Clinical Pharmacology and Therapeutics
|September 14, 2007
PubMed
Summary

Preventing cell death is key for treating ischemia-reperfusion injury. Targeting mitochondria, crucial in apoptosis, offers novel therapeutic strategies by modulating inner membrane permeability and morphology.

Area of Science:

  • Cardiovascular Science
  • Neuroscience
  • Cell Biology

Background:

  • Myocardial and cerebral infarction lead to significant functional deficits due to excessive cell death.
  • Ischemia-reperfusion injury necessitates therapeutic strategies focused on preventing cell death.

Purpose of the Study:

  • To highlight the critical role of mitochondria in ischemia-reperfusion.
  • To identify mitochondrial inner membrane permeability and morphology as potential therapeutic targets.

Main Methods:

  • Review of existing literature on cell death mechanisms in ischemia-reperfusion.
  • Analysis of the role of mitochondria in apoptotic pathways.

Main Results:

  • Mitochondria are central amplifiers of apoptotic cascades during ischemia-reperfusion.

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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

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Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy
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Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy

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Last Updated: Jul 11, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy
10:18

Triggering Cell Stress and Death Using Conventional UV Laser Confocal Microscopy

Published on: February 3, 2017

  • Alterations in mitochondrial inner membrane permeability and morphology are key regulated processes.

    • Conclusions:

    • Modulating mitochondrial function presents a promising therapeutic avenue for ischemia-reperfusion injury.
    • Targeting mitochondrial changes could reduce cell death and improve outcomes in infarction.