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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...
Apoptosis01:30

Apoptosis

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 reduction of the tissue.
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.
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...
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 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...

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Related Experiment Video

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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Conventional calpains and programmed cell death.

Paulina Łopatniuk1, Jacek M Witkowski

  • 1Department of Pathophysiology, Medical University of Gdańsk, Gdańsk, Poland. liliac@gumed.edu.pl

Acta Biochimica Polonica
|September 3, 2011
PubMed
Summary
This summary is machine-generated.

Calpains, calcium-dependent proteases, play a key role in programmed cell death and cancer. Further research into calpain activation is vital for developing new cancer therapies.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Medicine

Background:

  • Calpains are calcium-dependent cysteine proteases involved in programmed cell death.
  • Their roles in physiological and pathological processes, including cancer and immune function, are increasingly recognized.
  • Calpain involvement in central nervous system and cardiovascular diseases is also under investigation.

Purpose of the Study:

  • To elucidate the mechanisms of calpain function in apoptosis.
  • To summarize current knowledge on calpain activation pathways and their clinical significance.
  • To highlight calpains as potential therapeutic targets for various diseases.

Main Methods:

  • Literature review and synthesis of existing research on calpains and apoptosis.
  • Analysis of calpain involvement in different cellular processes and disease states.
  • Evaluation of the influence of calpain activity on drug-induced apoptosis.

Main Results:

  • Calpains are implicated in both normal and abnormal cell death, particularly in malignancies.
  • Evidence suggests calpain involvement in apoptosis execution in neurological and cardiovascular conditions.
  • Calpain activity significantly influences drug-induced apoptosis, underscoring their therapeutic potential.

Conclusions:

  • A comprehensive understanding of calpain activation and interactions is crucial for developing targeted therapies.
  • Calpains represent promising targets for pharmacological intervention in cancer and other diseases.
  • Further research is needed to translate the understanding of calpain pathways into clinical applications.