Abstract
Wound healing is a well-regulated complex process that occurs as a cellular response to injury and consists of four phases: hemostasis, inflammation, proliferation, and remodeling (1). Many factors, such as diabetes and obesity, interfere with these stages and lead to wound healing defect. Diabetes affects approximately 170 million people worldwide, including 20.8 million in the U.S., and by 2030 these numbers are projected to double (2). Impaired wound healing is a major clinical problem in patients with diabetes and is the leading cause of lower-extremity amputation and comorbidity associated with diabetes. Diabetic skin ulcers are estimated to occur in 15% of all patients with diabetes and 84% of all diabetes-related lower-leg amputations (3,4). Despite current treatments, one in four patients with diabetic ulcers will have a foot amputation. Therefore, new treatment strategies for healing diabetic skin ulcers are highly needed. Impaired or delayed wound healing in diabetes is characterized by impaired angiogenesis and vasculogenesis (5). Adult bone marrow progenitor cells, bone marrow–derived endothelial progenitor cells (BMPCs), can home to injured tissue and participate in the tissue repair regeneration process. However, in diabetes, BMPCs are dysfunctional (defective recruitment and reduced survival and proliferation) (6). The mechanism of bone marrow cell dysfunction in diabetes is not yet fully understood. Endoplasmic reticulum (ER), a multifunctional organelle involved in …
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