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<p>Amyotrophic lateral sclerosis (ALS) has been suggested to be associated with a reduced incidence of pressure ulcers, although the underlying mechanisms remain unclear. Here, we investigated pressure ulcer formation using a cutaneous ischemia–reperfusion (I/R) injury model in SOD1-G93A mice, a model of familial ALS. Under steady-state conditions, oxidative stress was markedly elevated in the dorsal root ganglia (DRG) and spinal cord compared with skin, accompanied by reduced PGP9.5<sup>+</sup> nerve fiber density in the skin. Following I/R injury, SOD1-G93A mice exhibited significantly attenuated ulcer formation during the early phase after reperfusion compared with wild-type mice. Quantitative PCR analysis demonstrated the reduced expression of oxidative stress-related genes, proinflammatory cytokines, and neuropeptides and their receptors in I/R skin site. Histological analyses revealed reduced infiltration of M1 macrophages, decreased 8-OHdG-positive oxidative DNA damage, and fewer apoptotic cells. Consistently, a denervation model showed reduced wound size after cutaneous I/R injury. Despite elevated oxidative stress in DRG and spinal cord, cutaneous oxidative and inflammatory responses were suppressed in SOD1-G93A mice. These findings suggest that impaired peripheral innervation attenuates neuropeptide-mediated inflammatory pathways, thereby reducing tissue injury following I/R and leading to decreased pressure ulcer formation in ALS.</p>

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Reduced neuropeptide signaling attenuates ischemia–reperfusion–induced pressure ulcer formation in SOD1-G93A mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月22日

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  • Akihiko Uchiyama,
  • Akiko Sekiguchi,
  • Yuta Inoue,
  • Shintaro Saito,
  • Keiji Kosaka,
  • Mayu Ohtaka,
  • Takeshi Araki,
  • Takayuki Shuto,
  • Azusa Ida,
  • Yoko Yokoyama,
  • Sachiko Ogino,
  • Ryoko Torii,
  • Yuki Watanuki,
  • Sei-ichiro Motegi

摘要

Amyotrophic lateral sclerosis (ALS) has been suggested to be associated with a reduced incidence of pressure ulcers, although the underlying mechanisms remain unclear. Here, we investigated pressure ulcer formation using a cutaneous ischemia–reperfusion (I/R) injury model in SOD1-G93A mice, a model of familial ALS. Under steady-state conditions, oxidative stress was markedly elevated in the dorsal root ganglia (DRG) and spinal cord compared with skin, accompanied by reduced PGP9.5+ nerve fiber density in the skin. Following I/R injury, SOD1-G93A mice exhibited significantly attenuated ulcer formation during the early phase after reperfusion compared with wild-type mice. Quantitative PCR analysis demonstrated the reduced expression of oxidative stress-related genes, proinflammatory cytokines, and neuropeptides and their receptors in I/R skin site. Histological analyses revealed reduced infiltration of M1 macrophages, decreased 8-OHdG-positive oxidative DNA damage, and fewer apoptotic cells. Consistently, a denervation model showed reduced wound size after cutaneous I/R injury. Despite elevated oxidative stress in DRG and spinal cord, cutaneous oxidative and inflammatory responses were suppressed in SOD1-G93A mice. These findings suggest that impaired peripheral innervation attenuates neuropeptide-mediated inflammatory pathways, thereby reducing tissue injury following I/R and leading to decreased pressure ulcer formation in ALS.