Diabetes mellitus increases the risk and accelerates the course of peripheral artery disease, making patients more susceptible to ischemic events and infections and delaying tissue healing. Current understanding of pathogenic mechanisms is mainly based on the negative influence of diabetes mellitus on atherosclerotic disease and inflammation. In recent years, the novel concept that diabetes mellitus can impinge on endogenous regenerative processes has been introduced. Diabetes mellitus affects regeneration at the local level, disturbing proper angiogenesis, collateral artery formation, and muscle repair. Recent evidence indicates that an impairment in vascular mural cells, alias pericytes, may participate in diabetic peripheral vasculopathy. Moreover, the bone marrow undergoes a global remodeling, consisting of microvessels and sensory neurons rarefaction and fat accumulation, which creates a hostile microenvironment for resident stem cells. Bone marrow remodeling is also responsible for detrimental systemic effects. In particular, the aid of reparative cells from the bone marrow is compromised: these elements are released in an improper manner and become harmful vectors of inflammatory and antiangiogenic molecules and noncoding RNAs. This new understanding of impaired regeneration is inspiring new therapeutic options for the treatment of ischemic complications in people with diabetes mellitus.

中文翻译：

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再生障碍导致糖尿病性外周动脉疾病的不良结果。

糖尿病增加了患病风险并加速了外周动脉疾病的进程，使患者更易受缺血事件和感染的影响，并延迟了组织的愈合。当前对致病机制的理解主要基于糖尿病对动脉粥样硬化疾病和炎症的负面影响。近年来，已经提出了糖尿病可以影响内源性再生过程的新概念。糖尿病会影响局部水平的再生，干扰正常的血管生成，侧支动脉形成和肌肉修复。最近的证据表明，血管壁细胞的损伤（别名周细胞）可能参与了糖尿病性周围血管病。而且，骨髓经历了整体重塑，由微血管和感觉神经元稀疏和脂肪积累组成，这为驻留干细胞创造了不利的微环境。骨髓重塑也造成有害的全身作用。特别地，来自骨髓的修复细胞的帮助受到损害：这些元素以不适当的方式释放，并成为炎性和抗血管生成分子以及非编码RNA的有害载体。对再生受损的新认识为治疗糖尿病患者的缺血性并发症提供了新的治疗选择。骨髓修复细胞的帮助受到损害：这些元素以不适当的方式释放，并成为炎性和抗血管生成分子以及非编码RNA的有害载体。对再生受损的新认识为治疗糖尿病患者的缺血性并发症提供了新的治疗选择。骨髓修复细胞的帮助受到损害：这些元素以不适当的方式释放，并成为炎性和抗血管生成分子以及非编码RNA的有害载体。对再生受损的新认识为治疗糖尿病患者的缺血性并发症提供了新的治疗选择。