Abstract
Pressure ulcers are preventable, yet highly prevalent, chronic wounds that have significant patient morbidity and high healthcare costs. Like other chronic wounds, they are characterized by impaired wound healing due to dysregulated immune processes. This review will highlight key biochemical pathways in the pathogenesis of pressure injury and how this signaling leads to impaired wound healing. This review is the first to comprehensively describe the current literature on microRNA (miRNA, miR) regulation of pressure ulcer pathophysiology.
Highlights
Many of the pathophysiologic pathways in the development of chronic wounds are regulated by miRNAs, and the implications of miRNA dysregulation in pressure injury are of growing interest
The effects of miR-21 on dysregulated immune response and healing in diabetic wounds have been well characterized [93,94,95]. miR-21 is upregulated during the early phases of diabetic wound healing, and over-expression of miR-21 leads to increased expression of the proinflammatory cytokines IL-1β, TNFα, inducible nitric oxide synthase, and IL-6 and to the promotion of a pro-inflammatory M1 macrophage phenotype [27]
MicroRNAs have been described in the pathogenesis and treatment of chronic wounds, but their specific roles in the pathogenesis of pressure ulcers have not been reviewed previously
Summary
Pressure ulcers are chronic wounds associated with significant morbidity and are a substantial burden to the healthcare system. Patients who develop pressure ulcers have significant psychosocial burden associated with the disease, including increased anxiety and feelings of social isolation, in addition to the physical morbidity associated with prolonged hospital stays and increased risk of infection [7]. The average hospital length of stay for patients diagnosed with a pressure ulcer is three times that of patients who do not develop pressure ulcers, inciting additional care-related costs of USD 8200–25,000 per stay and over USD 11 billion annually [5,8,9,10]
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