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Related Concept Videos

Caspases01:24

Caspases

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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...
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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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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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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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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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.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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Related Experiment Video

Updated: Feb 24, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Caspases, Cell Death and Diabetic Nephropathy.

Elena Bălăşescu, Daniela Adriana Ion, Mirela Cioplea

    Romanian Journal of Internal Medicine = Revue Roumaine De Medecine Interne
    |March 5, 2016
    PubMed
    Summary

    Diabetic nephropathy affects a quarter of diabetes patients, with cell death pathways like apoptosis being key but understudied mechanisms. Further research into renal cell death types and caspases is crucial for understanding disease progression.

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    Area of Science:

    • Nephrology
    • Cell Biology
    • Endocrinology

    Background:

    • Diabetes affects 9% of the global population, leading to significant mortality.
    • Diabetic nephropathy, a common complication, impacts approximately 25% of diabetes patients.
    • Similarities in physiopathology and cell injury exist between Type 1 and Type 2 diabetic nephropathy.

    Purpose of the Study:

    • To highlight the understudied role of cell death in diabetic nephropathy.
    • To explore the mechanisms of renal cellular loss in diabetic kidney disease.
    • To emphasize the need for elucidating cell death types and caspase involvement.

    Main Methods:

    • Review of existing literature on diabetic nephropathy and cell death.
    • Analysis of physiopathology and ultrastructural changes in renal cells.
    • Discussion of the known roles of apoptosis and caspases in cellular processes.

    Main Results:

    • Cell death represents a significant, yet under-investigated, pathogenic mechanism in diabetic nephropathy.
    • Multiple stimuli can trigger apoptosis signaling, involving regulatory proteins with dual roles.
    • The specific types and proportions of cell death in renal tissue remain largely undefined.

    Conclusions:

    • Cell death is a critical factor in the development and progression of diabetic nephropathy.
    • Caspases, cysteine proteases involved in apoptosis and inflammation, play a role in diabetic kidney disease.
    • Further research is needed to fully elucidate the cell death pathways and their regulation in diabetic nephropathy.