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After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
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Protocol to Create Chronic Wounds in Diabetic Mice
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Senescence Programs Shape the Chronic Wound Microenvironment.

Maria Shvedova1, Minsung Cho1, Jeroen Eyckmans2,3

  • 1Division of Plastic and Reconstructive Surgery, Department of Surgery, Boston University School of Medicine, Boston, Massachusetts, USA.

Advances in Wound Care
|April 12, 2026
PubMed
Summary
This summary is machine-generated.

Cellular senescence, a state of irreversible cell growth arrest, drives chronic inflammation and impairs healing in wounds like diabetic foot ulcers. Targeting these senescent cells offers potential therapeutic strategies for nonhealing conditions.

Keywords:
cellular senescencechronic woundsfibroblast senescencesenescence-associated secretory phenotypewound healing

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Area of Science:

  • Wound healing research
  • Cellular biology
  • Immunology

Background:

  • Chronic wounds exhibit impaired healing and persistent inflammation.
  • Cellular senescence, characterized by a pro-inflammatory secretory phenotype, is implicated in nonhealing wound states.
  • Senescent cells disrupt tissue regeneration and promote inflammation.

Purpose of the Study:

  • To investigate the role of cellular senescence in chronic wound pathogenesis.
  • To explore therapeutic strategies targeting senescent cells for improved wound healing.

Main Methods:

  • Single-cell RNA sequencing and spatial transcriptomics to identify senescent cell subsets.
  • Preclinical models of delayed wound healing to test senolytic interventions.

Main Results:

  • Senescent fibroblasts and immune cells contribute to impaired remodeling in chronic wounds.
  • Senescence plays context-dependent roles, beneficial in acute healing but detrimental in chronic wounds.
  • Current markers for senescence are often nonspecific, complicating interpretation.

Conclusions:

  • Further research using advanced single-cell and spatial techniques is needed to define senescent cell populations and their dynamics.
  • Understanding senescent cell interactions with tissue components is crucial for developing targeted therapies.
  • Precisely timed, cell-specific interventions are required to improve chronic wound outcomes.