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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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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...
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Necrosis01:16

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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Apoptosis01:30

Apoptosis

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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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Regulation of Angiogenesis and Blood Supply01:24

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Autophagic Cell Death01:18

Autophagic Cell Death

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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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The Extrinsic Apoptotic Pathway01:17

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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...
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Related Experiment Video

Updated: Sep 14, 2025

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
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The relationship between programmed cell death and vascular calcification.

Jie Zheng1, Zhengjie Lin1, Xiaolin Zhong1

  • 1The First Affiliated Hospital, Institute of Endocrinology and Metabolism, Center for Clinical Research in Diabetes, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Frontiers in Cardiovascular Medicine
|July 25, 2025
PubMed
Summary
This summary is machine-generated.

Vascular calcification, a contributor to cardiovascular diseases, is driven by programmed cell death. Understanding these cell death mechanisms offers new therapeutic targets for heart conditions.

Keywords:
atherosclerosisdiabetic angiopathyprogrammed cell deathsignaling pathwaysvascular calcification

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Area of Science:

  • Cardiovascular Biology
  • Cellular Pathology

Background:

  • Vascular calcification (VC) is linked to cardiovascular diseases like atherosclerosis, hypertension, and diabetic angiopathy.
  • Programmed cell death, including apoptosis, autophagy, pyroptosis, and ferroptosis, is integral to VC progression.

Purpose of the Study:

  • To explore the role of programmed cell death in vascular calcification.
  • To investigate the signaling pathways regulating these cellular processes in VC.

Main Methods:

  • Review of existing literature on vascular calcification and programmed cell death.
  • Analysis of signaling pathways (e.g., Wnt/β-catenin, NF-κB) involved in VC.

Main Results:

  • Programmed cell death pathways are key mediators in the development and progression of vascular calcification.
  • Signaling pathways like Wnt/β-catenin and NF-κB intricately regulate these cell death processes.

Conclusions:

  • Understanding programmed cell death mechanisms in VC is crucial.
  • Targeting these cellular processes may lead to novel therapeutic strategies for cardiovascular diseases.