Background: With the increasing incidence of diabetes, diabetic foot ulcer(DFU) has become one of the most common and serious complications in people with diabetes. DFU is associated with significant morbidity and mortality, and can also result in significant economic, social and public health burdens. Due to peripheral neuropathy, peripheral vascular disease, hyperglycemic environment, inflammatory disorders and other factors, the healing of DFU is impaired or delayed, resulting in the formation of diabetic chronic refractory ulcer. Because of these pathological abnormalities in DFU, it may be difficult to promote wound healing with conventional therapies or antibiotics, whereas platelet-rich plasma(PRP) can promote wound healing by releasing various bioactive molecules stored in platelets, making it more promising than traditional antibiotics. Therefore, the purpose of this systematic review is to summarize and analyze the efficacy of PRP in the treatment of DFU.Methods: A literature search was undertaken in PubMed, CNKI, EMB-ASE, the Cochrane Library, the WanFang Database and the WeiPu Database by computer. Included controlled studies evaluating the efficacy of PRP in the treatment of diabetic foot ulcers. The data extraction and assessment are on the basis of PRISMA.Results: Twenty studies were evaluated, and nineteen measures for the evaluation of the efficacy of PRP in DFU treatment were introduced by eliminating relevant duplicate measures. The efficacy measures that were repeated in various studies mainly included the rate of complete ulcer healing, the percentage of ulcer area reduction, the time required for ulcer healing, wound complications (including infection rate, amputation rate, and degree of amputation), the rate of ulcer recurrence, and the cost and duration of hospitalization for DFU, as well as subsequent survival and quality of life scores. One of the most important indicators were healing rate, ulcer area reduction and healing time. The meta-analysis found that PRP was significantly improve the healing rate(OR = 4.37, 95% CI 3.02-6.33, P < 0.001) and shorten the healing time(MD = -3.21, 95% CI -3.83 to -2.59,P < 0.001)of patients with DFU when compared to the conventional treatment, but there was no significant difference in reducing the of ulcer area(MD = 5.67, 95% CI -0.77 to 12.11,P =0.08>0.05 ).Conclusion: The application of PRP to DFU can improve ulcer healing rate and shorten ulcer healing time, but more clinical data are needed to clarify some efficacy measures. At the same time, a standardized preparation process for PRP is essential.

Introduction: As a severe and specific neurovascular complication of type 2 diabetes mellitus (T2DM), diabetic retinopathy (DR) remains the leading cause of vision loss and preventable blindness in adults aged 20 to 74. The pathogenesis of DR is not completely understood, however, studies indicate that chronic inflammation plays a significant role. Emerging evidence suggests that the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), and the monocyte-to-lymphocyte ratio (MLR) are novel potential inflammatory response markers. The purpose of this study was to investigate the relationships between the NLR, PLR, MLR, and DR. Patients and Methods: 290 patients who had been diagnosed with T2DM participated in the study. Patients were categorized into three groups: 142 control subjects with T2DM, 124 subjects with nonproliferative diabetic retinopathy (NPDR), and 24 patients with proliferative diabetic retinopathy (PDR). Characteristics, laboratory data, as well as NLR, PLR and MLR levels of the study groups were compared. Results: In patients with DR, the median NLR, PLR, and MLR were significantly higher than in patients without DR (p = 0.012, p < 0.001, and p = 0.043, respectively). In the post hoc analysis, there was no correlation between the severity of retinopathy and the increase in NLR or PLR. Multiple logistic regression revealed that the PLR was an independent risk factor for DR (odds ratio [OR]: 1.020, 95% confidence interval [CI]: 1.010– 1.029 p = 0.026). Based on the receiver operating characteristic (ROC) curve, the cutoff value of PLR as an indicator for diagnosing DR was estimated to be 129.65, with a sensitivity and specificity of 53.4% and 76.1%, respectively, and an area under the curve of 0.668 (95% CI: 0.605– 0.730, p < 0.001). Conclusion: Our findings suggest that PLR may be an independent risk factor for evaluating DR in type 2 diabetes patients.

Glucose and lipid metabolism disorders caused by insulin resistance (IR) can lead to metabolic disorders such as diabetes, obesity, and the metabolic syndrome. Early and targeted intervention of IR is beneficial for the treatment of various metabolic disorders. Although significant progress has been made in the development of IR drug therapies, the state of the condition has not improved significantly. There is a critical need to identify novel therapeutic targets. Mitophagy is a type of selective autophagy quality control system that is activated to clear damaged and dysfunctional mitochondria. Mitophagy is highly regulated by various signaling pathways, such as the AMPK/mTOR pathway which is involved in the initiation of mitophagy, and the PINK1/Parkin, BNIP3/Nix, and FUNDC1 pathways, which are involved in mitophagosome formation. Mitophagy is involved in numerous human diseases such as neurological disorders, cardiovascular diseases, cancer, and aging. However, recently, there has been an increasing interest in the role of mitophagy in metabolic disorders. There is emerging evidence that normal mitophagy can improve IR. Unfortunately, few studies have investigated the relationship between mitophagy and IR. Therefore, we set out to review the role of mitophagy in IR and explore whether mitophagy may be a potential new target for IR therapy. We hope that this effort serves to stimulate further research in this area.

Denosumab is a recently developed anti-osteoporosis agent widely applied in the treatment of osteoporosis in postmenopausal women. As a potent inhibitor of bone resorption, it significantly increases bone mineral density, lowers elevated bone turnover rates, and reduces fracture risk. Because denosumab does not bind to the bone matrix, its effects decrease rapidly after discontinuation, a process commonly known as the “rebound effect.” Research has shown that administering zoledronic acid after stopping denosumab can help preserve bone density and reduce the likelihood of vertebral fractures. However, the exact effectiveness of this sequential approach and the factors influencing it, including the duration of prior denosumab treatment, timing, and frequency of zoledronic acid administration, remain insufficiently understood. To address these uncertainties, this review evaluates the effects of sequential zoledronic acid therapy on subsequent changes in bone density, bone turnover markers, fracture risk, and adverse reactions. We also examined in detail the dosage strategies, administration intervals of zoledronic acid, and length of preceding denosumab use across studies, aiming to assist clinicians in designing more evidence-based and clinically relevant sequential treatment protocols.