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<p>The recent study by Santos-De-La-Mata et al. (Angiogenesis 28(4): 482025, 2025) provides critical evidence that adipose-derived stem cells (ASCs) from patients with chronic spinal cord injury (SCI) and pressure injuries (PIs) exhibit significantly impaired vasculogenic potential.1 Their comparative analysis revealed deficits in key pro-angiogenic functions, including reduced proliferation, migration, tube formation, and secretion of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in SCI/PI-derived ASCs compared to healthy controls. These in vitro findings were corroborated by a diminished capacity to support neovascularization in an in vivo Matrigel plug assay. This cellular dysfunction underscores a fundamental mechanism contributing to refractory wound healing in this patient population and critically challenges the efficacy of autologous ASC-based therapies. This analysis discusses these findings in the context of chronic inflammatory microenvironments and epigenetic regulation,2,3 and explores potential strategies to overcome this impairment, including allogeneic cell sources4,5 and pre-conditioning techniques to rejuvenate patient-derived cells.6 The work of Santos-De-La-Mata et al. establishes a vital foundation for developing more effective, personalized regenerative medicine approaches for complex chronic wounds.</p>

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Dysfunctional vasculogenesis in adipose-derived stem cells from chronic spinal cord injury patients: implications for autologous cell therapy

  • 期刊论文

  • 发表日期：

    2025年10月10日

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  • DuJiang Yang,
  • Lin Yang,
  • Junjie Chen,
  • Zihe Wang,
  • Shuang Wang,
  • Jiexiang Yang,
  • GuoYou Wang

摘要

The recent study by Santos-De-La-Mata et al. (Angiogenesis 28(4): 482025, 2025) provides critical evidence that adipose-derived stem cells (ASCs) from patients with chronic spinal cord injury (SCI) and pressure injuries (PIs) exhibit significantly impaired vasculogenic potential.1 Their comparative analysis revealed deficits in key pro-angiogenic functions, including reduced proliferation, migration, tube formation, and secretion of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in SCI/PI-derived ASCs compared to healthy controls. These in vitro findings were corroborated by a diminished capacity to support neovascularization in an in vivo Matrigel plug assay. This cellular dysfunction underscores a fundamental mechanism contributing to refractory wound healing in this patient population and critically challenges the efficacy of autologous ASC-based therapies. This analysis discusses these findings in the context of chronic inflammatory microenvironments and epigenetic regulation,2,3 and explores potential strategies to overcome this impairment, including allogeneic cell sources4,5 and pre-conditioning techniques to rejuvenate patient-derived cells.6 The work of Santos-De-La-Mata et al. establishes a vital foundation for developing more effective, personalized regenerative medicine approaches for complex chronic wounds.