Pressure injuries (PIs), also known as bedsores or pressure ulcers, are a major cause of death and morbidity in the elderly. The serine protease, Granzyme B (GzmB), contributes to skin aging and impaired wound healing. Aging is a major risk factor for PIs; thus, the role of GzmB in PI pathogenesis was investigated. GzmB levels in human PI tissue and wound fluids were markedly elevated. A causative role for GzmB was assessed in GzmB knockout (GzmB−/−) and wild-type (WT) mice using a murine model of PI. An apolipoprotein E knockout (ApoE−/−) model of aging and vascular dysfunction was also utilized to assess GzmB in a relevant age-related model better resembling tissue perfusion in the elderly. PI severity displayed no difference between young GzmB−/− and WT mice. However, in aged mice, PI severity was reduced in mice lacking GzmB. Mechanistically, GzmB increased vascular wall inflammation and impaired extracellular matrix remodeling. Together, GzmB is an important contributor to age-dependent impaired PI healing.

压力伤害（PI），也称为褥疮或压力溃疡，是老年人死亡和发病的主要原因。丝氨酸蛋白酶Granzyme B（GzmB）有助于皮肤衰老和伤口愈合受损。老化是效绩指标的主要风险因素；因此，研究了GzmB在PI发病机理中的作用。人PI组织和创面液中的GzmB水平显着升高。使用PI鼠模型在GzmB基因敲除（GzmB-/-）和野生型（WT）小鼠中评估了GzmB的致病作用。衰老和血管功能障碍的载脂蛋白E基因敲除（ApoE-/-）模型也被用于评估与年龄相关的模型中的GzmB，该模型更类似于老年人的组织灌注。PI严重程度显示，年轻的GzmB-/-和WT小鼠之间没有差异。但是，在老年小鼠中，缺乏GzmB的小鼠的PI严重性降低。机械上，GzmB增加血管壁炎症和受损的细胞外基质重塑。总之，GzmB是依赖于年龄的受损PI愈合的重要贡献者。