No abstract

Diabetic foot ulcers (DFU), one of the most serious complications of diabetes, are essentially chronic, nonhealing wounds caused by diabetic neuropathy, vascular disease, and bacterial infection. Given its pathogenesis, the DFU microenvironment is rather complicated and characterized by hyperglycemia, ischemia, hypoxia, hyperinflammation, and persistent infection. However, the current clinical therapies for DFU are dissatisfactory, which drives researchers to turn attention to advanced nanotechnology to address DFU therapeutic bottlenecks. In the last decade, a large number of multifunctional nanosystems based on the microenvironment of DFU have been developed with positive effects in DFU therapy, forming a novel concept of “DFU nanomedicine”. However, a systematic overview of DFU nanomedicine is still unavailable in the literature. This review summarizes the microenvironmental characteristics of DFU, presents the main progress of wound healing, and summaries the state‐of‐the‐art therapeutic strategies for DFU. Furthermore, the main challenges and future perspectives in this field are discussed and prospected, aiming to fuel and foster the development of DFU nanomedicines successfully.

Background: Tripterygium wilfordii Hook F can cause adverse effects (AEs) in clinical application and may be harmful to human health. This study aim to summarize the AEs caused by T. wilfordii tgpolyglycoside (TWP), the most common preparation of T. wilfordii Hook F for clinical use. Methods: The Cochrane Library, EMBASE, PubMed, and Web of Science were searched to identify potential articles on this topic. All single-arm trials, controlled clinical trials, and randomized controlled trials were selected and summarized. Meta-regression was used to determine the sources of heterogeneity, and subgroups were used to identify factors leading to AEs. Results: Forty-six studies, comprising 25 randomized controlled trials, 13 controlled clinical trials, and 8 single-arm trials, were included in this meta-analysis, representing 2437 enrolled TWP-treated participants. Combined intervention, drug dosage, medication treatment, pharmaceutical manufacturers, and specific organ toxicity were identified as potential factors leading to TWP-induced AEs in this meta-analysis. In patients treated with TWP, the global incidence of AEs was 30.75% (95% confidence interval [21.18–40.33], I 2 = 97%), and that of severe grade AEs was 4.68% (95% confidence interval [0.00–12.72], I 2 = 53%). Organ-specific analyses indicated that TWP treatment elicited intestinal toxicity, reproductive toxicity, hepatotoxicity, nephrotoxicity, hematotoxicity, cutaneous toxicity, and other damages. The AEs analyzed in the subgroups of combined intervention, drug dosage, medication treatment, and pharmaceutical manufacturers were considered as primary outcomes, and organic-specific AEs were considered as secondary outcomes. Conclusions: The occurrence of TWP-induced AEs was systemic, organ-specific, and related to medication course, combined intervention, and drug dosage.