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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...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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,...
Necrosis01:16

Necrosis

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”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...

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Related Experiment Video

Updated: Jun 2, 2026

Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
08:26

Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death

Published on: October 31, 2017

Mitochondrial dysfunction links ceramide activated HRK expression and cell death.

Farhan Rizvi1, Tom Heimann, Anja Herrnreiter

  • 1Department of Ophthalmology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America. frizvi@mcw.edu

Plos One
|April 13, 2011
PubMed
Summary

Ceramide induces human corneal stromal fibroblast death by causing mitochondrial dysfunction and upregulating the harikari gene (HRK). HRK knockdown reduces ceramide-induced cell death, highlighting its role in corneal wound healing.

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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Cell death is crucial for corneal wound healing following injury.
  • The precise molecular mechanisms of corneal stromal cell death after injury, such as following LASIK surgery, are not fully understood.
  • Ceramide has been implicated in stromal cell death post-LASIK.

Purpose of the Study:

  • To investigate the mechanism by which C6 ceramide induces cell death in human corneal stromal fibroblasts (HCSF).
  • To elucidate the role of ceramide in corneal stromal cell death and its potential implications for wound healing.

Main Methods:

  • HCSF cultures were treated with C6 ceramide or a control.
  • Cell death was assessed using Live/Dead staining, Annexin V, caspase activation, and TUNEL assays.
  • Mitochondrial function, gene expression (qPCR, Western blotting), and protein interactions were analyzed.

Main Results:

  • Ceramide induced mitochondrial dysfunction, evidenced by reduced MTT, cytochrome c release, increased ROS, and loss of mitochondrial membrane potential.
  • Ceramide triggered the expression of the harikari gene (HRK) and JNK phosphorylation, leading to HRK translocation to mitochondria.
  • HRK interacted with p32 and BAD in mitochondria, and HRK knockdown significantly reduced ceramide-induced cell death.

Conclusions:

  • Ceramide induces human corneal stromal fibroblast death via HRK-mediated mitochondrial dysfunction.
  • This pathway is a key mechanism contributing to corneal stromal cell death and potentially corneal wound healing.