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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.
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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 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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A guide to cell death pathways.

Junying Yuan1,2, Dimitry Ofengeim3

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Programmed cell death, including apoptosis, necroptosis, and pyroptosis, is crucial in health and disease. This review details major cell death mechanisms, their regulation, and disease relevance.

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Pathology

Background:

  • Regulated cell death, or programmed cell death, is vital for organismal health and disease processes.
  • Key programmed cell death pathways include apoptosis, necroptosis, and pyroptosis, each involving distinct molecular machinery.
  • Disruptions in cellular homeostasis can also trigger non-programmed cell death, such as excitotoxicity, ferroptosis, and lysosomal cell death.

Purpose of the Study:

  • To provide a comprehensive overview of major cell death mechanisms.
  • To highlight recent advancements in understanding the complex regulation and execution of these pathways.
  • To discuss the relevance of diverse cell death modes in human diseases.

Main Methods:

  • Review of existing literature on programmed and non-programmed cell death.
  • Analysis of molecular regulators and signaling pathways involved in cell death.
  • Integration of findings related to the pathological implications of cell death.

Main Results:

  • Apoptosis involves caspase cascades, while pyroptosis relies on caspase-activated gasdermins forming membrane pores.
  • Necroptosis is a caspase-independent pathway regulated by RIPK3 and MLKL, inhibited by caspase-8.
  • Non-programmed cell death modes arise from disruptions in cellular homeostasis, affecting ionic balance, redox state, and lysosomal function.

Conclusions:

  • Understanding the intricate network of cell death pathways is essential for deciphering disease pathogenesis.
  • Targeting specific cell death mechanisms holds therapeutic potential for various human diseases.
  • Further research into the interplay between different cell death modalities will advance the field.