Purpose Of Review: Defective wound healing is one of the most prominent clinical manifestations of both type 1 and type 2 diabetes. As the global rates of diabetes increase, a detailed understanding of the molecular and cellular defects that give rise to unresolved inflammation and delayed wound healing in diabetes is urgently required. Emerging evidence indicates that timely resolution of inflammation is mediated in part by endogenous proresolving lipid mediators, such as resolvins. Here, we review recent advances in the area of resolution and diabetes and highlight the potential of novel proresolving strategies for promoting wound healing in diabetes.
Recent Findings: Macrophage dysfunction is a critical underlying feature of altered wound healing in diabetic patients. This is associated with defective clearance of apoptotic cells, increased risk of infection, and altered angiogenesis. Diabetes and obesity are associated with chronic inflammation and altered biosynthesis of bioactive lipid mediators that promote the resolution of inflammation. Stimulating resolution with proresolving lipid mediators improves metabolic parameters in diabetes, blunts systemic inflammation, restores defective macrophage phagocytosis, and accelerates wound healing in animal models of obesity and diabetes.
Summary: Stimulating resolution with proresolving lipid mediators may represent a novel strategy for promoting wound healing in diabetes.
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http://dx.doi.org/10.1097/MED.0b013e3283514e00 | DOI Listing |
Biochem Genet
December 2024
Department of Obstetrics and Gynecology, Wuhan Third Hospital (Tongren Hospital of Wuhan University), No.216, Guanshan Avenue, Hongshan District, Wuhan, 430074, Hubei, China.
Cisplatin, a platinum-based chemotherapeutic agent, can be used to treat cervical cancer (CC), but cisplatin resistance is increased during the cisplatin treatment. Long non-coding RNA PGM5-AS1 reportedly participates in CC tumorigenesis; however, its role in CC patients with cisplatin resistance has not been revealed. The present aimed to examine the role of PGM5-AS1 in modulating cisplatin resistance in CC.
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December 2024
Department of Orthopaedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Chronic complete spinal cord injury (SCI) is difficult to treat because of scar formation and cavitary lesions. While human iPS cell-derived neural stem/progenitor cell (hNS/PC) therapy shows promise, its efficacy is limited without the structural support needed to address cavitary lesions. Our study investigated a combined approach involving surgical scar resection, decellularized extracellular matrix (dECM) hydrogel as a scaffold, and hNS/PC transplantation.
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December 2024
Department of Ultrasound, The First Hospital of Hunan University of Chinese Medicine, Hunan University of Chinese Medicine, Changsha, 410021, Hunan, People's Republic of China.
To develop and validate a nomogram for predicting the risk of adverse events (intraoperative massive haemorrhage or retained products of conception) associated with the termination of Caesarean scar pregnancy (CSP). Data were retrospectively collected from patients diagnosed with CSP who underwent Dilation and Curettage (D&C) at two hospitals. This data was divided into internal and external cohorts for analysis.
View Article and Find Full Text PDFAesthetic Plast Surg
December 2024
Dallas Plastic Surgery Institute, 9101 N Central Expy, Dallas, Texas, 75225, USA.
Introduction: Continued interest in the optimization of recovery in aesthetics has led to the exploration of adjunctive therapies. Hyperbaric oxygen therapy (HBOT) serves as one such therapy that may have an impact in this field. HBOT is hypothesized to improve ischemia, reduce swelling, and minimize secondary hypoxic tissue damage.
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December 2024
Department of Dermatology, Hebei Medical University Third Hospital, 139 Ziqiang Road, Shijiazhuang, 050000, Hebei, China.
To investigate CHD1L's impacts and molecular processes in hypoxic cutaneous squamous cell carcinoma. Monoclonal proliferation assays and CCK-8 were used to detect the proliferation capacity of A431 cells and Colon16 cells; wound healing experiments and Transwell assays were used to examine the migration and invasion capacity of A431 cells and Colon16 cells; angiogenesis experiments were conducted to assess the influence of A431 cells on angiogenesis; a nude mouse tumor xenograft experiment and HE staining were utilized to evaluate the impact of CHD1L on the progression of cutaneous squamous cell carcinoma; western blot analysis was performed to detect the expression of p-PI3K, p-AKT, and PD-L1 in A431 cells, as well as CD9, TSG101, PD-L1 in exosomes, and CD206, Arginase-1, iNOS, IL-1β, p-AKT, p-mTOR, VEGF, COX-2, MMP2, MMP9, p-ERK1/2 in tumor-associated macrophages. Under hypoxic conditions, CHD1L promoted the proliferation, migration, invasion, and angiogenesis of cutaneous squamous cell carcinoma.
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