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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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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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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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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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Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
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How Do Red Blood Cells Die?

Perumal Thiagarajan1,2, Charles J Parker3, Josef T Prchal4

  • 1Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, United States.

Frontiers in Physiology
|April 1, 2021
PubMed
Summary
This summary is machine-generated.

Macrophages efficiently clear aged red blood cells, but the exact molecular signals triggering this process remain unclear. Future research using advanced techniques may illuminate red blood cell senescence and clearance mechanisms.

Keywords:
Band 3complementphosphatidylserine (PS) exposurered cell deformabilityspleen

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Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Red blood cells have a lifespan of approximately 120 days before clearance by macrophages.
  • Macrophage phagocytosis of erythrocytes is highly efficient, preventing hemoglobin release.
  • The precise molecular mechanisms for macrophage recognition of senescent red blood cells are not fully understood.

Purpose of the Study:

  • To review recent data on the clearance mechanisms of senescent red blood cells.
  • To highlight the ongoing challenges in understanding red blood cell destruction.
  • To discuss potential future directions for research in this field.

Main Methods:

  • Review of existing literature on red blood cell senescence and clearance.
  • Discussion of proposed recognition mechanisms, including neoantigen expression, phosphatidylserine exposure, and decreased deformability.
  • Consideration of emerging techniques such as in vivo red blood cell labeling and proteomics.

Main Results:

  • Several physicochemical changes occur in aging red blood cells, but their causal role in clearance is not definitively established.
  • Current understanding of the molecular details of red blood cell clearance remains incomplete.
  • Recent advances in research methodologies are expected to enhance future investigations.

Conclusions:

  • The molecular basis for macrophage recognition of senescent erythrocytes requires further elucidation.
  • Advanced techniques like in vivo labeling and proteomics hold promise for future discoveries.
  • Continued research is crucial for a comprehensive understanding of red blood cell homeostasis and destruction.