Objective. Rhizoma Coptidis is an herb that has been frequently used in many traditional formulas for the treatment of diabetic mellitus (DM) over thousands of years. Berberine, the main active component of Rhizoma Coptidis, has been demonstrated to have the potential effect of hypoglycemia. To determine the potential advantages of berberine for diabetic care, we conducted this systematic review and meta‐analysis to examine the efficacy and safety of berberine in the treatment of patients with type 2 DM. Methods. Eight databases including PubMed, Embase, Web of Science, the Cochrane library, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Database (SinoMed), Wanfang Database, and Chinese VIP Information was searched for randomized controlled trials (RCTs) reporting clinical data regarding the use of berberine for the treatment of DM. Publication qualities were also considered to augment the credibility of the evidence. Glycemic metabolisms were the main factors studied, including glycosylated hemoglobin (HbA1c), fasting plasm glucose (FPG), and 2‐hour postprandial blood glucose (2hPG). Insulin resistance was estimated by fasting blood insulin (FINS), homeostasis model assessment‐insulin resistance (HOMA‐IR), and body mass index (BMI). Lipid profiles were also assessed, including triglyceride (TG), total cholesterol (TC), low‐density lipoprotein (LDL), and high‐density lipoprotein (HDL), along with inflammation factors such as C‐reactive protein (CRP), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α). Serum creatinine (Scr), blood urea nitrogen (BUN), and adverse events were applied to evaluate the safety of berberine. Results. Forty‐six trials were assessed. Analysis of berberine applied alone or with standard diabetic therapies versus the control group revealed significant reductions in HbA1c (MD = −0.73; 95% CI (−0.97, −0.51)), FPG (MD = −0.86, 95% CI (−1.10, −0.62)), and 2hPG (MD = −1.26, 95% CI (−1.64, −0.89)). Improved insulin resistance was assessed by lowering FINS (MD = −2.05, 95% CI (−2.62, −1.48)), HOMA‐IR (MD = −0.71, 95% CI (−1.03, −0.39)), and BMI (MD = −1.07, 95% CI (−1.76, −0.37)). Lipid metabolisms were also ameliorated via the reduction of TG (MD = −0.5, 95% CI (−0.61, −0.39)), TC (MD = 0.64, 95% CI (−0.78, −0.49)), and LDL (MD = 0.86, 95% CI (−1.06, −0.65)) and the upregulation of HDL (MD = 0.17, 95% CI (0.09, 0.25)). Additionally, berberine improved the inflammation factor. Conclusion. There is strong evidence supporting the clinical efficacy and safety of berberine in the treatment of DM, especially as an adjunctive therapy. In the future, this may be used to guide targeted clinical use of berberine and the development of medications seeking to treat patients with T2DM and dyslipidemia.

Diabetic nephropathy (DN) is a progressive microvascular diabetic complication. Growing evidence shows that persistent mitochondrial dysfunction contributes to the progression of renal diseases, including DN, as it alters mitochondrial homeostasis and, in turn, affects normal kidney function. Pharmacological regulation of mitochondrial networking is a promising therapeutic strategy for preventing and restoring renal function in DN. In this review, we have surveyed recent advances in elucidating the mitochondrial networking and signaling pathways in physiological and pathological contexts. Additionally, we have considered the contributions of nontraditional therapy that ameliorate mitochondrial dysfunction and discussed their molecular mechanism, highlighting the potential value of nontraditional therapies, such as herbal medicine and lifestyle interventions, in therapeutic interventions for DN. The generation of new insights using mitochondrial networking will facilitate further investigations on nontraditional therapies for DN.

Membranous nephropathy (MN) is an organ-restricted autoimmune disease mainly caused by circulating autoantibodies against podocyte antigens, including the M-type phospholipase A2 receptor (PLA2R) and thrombospondin domain-containing 7A (THSD7A). Antibodies against PLA2R are present in 70%–80% and against THSD7A in 2% of adult patients, which provides a paradigm shift in molecular diagnosis and management monitoring. Both antigens share some similar characteristics: they are expressed by podocytes and have wide tissue distributions; they are bound by autoantibodies only under nonreducing conditions, and the subtype of most autoantibodies is IgG4. However, the factors triggering autoantibody production as well as the association among air pollution, malignancy, and the pathogenesis of MN remain unclear. In this review, we discuss the similarity between the pathological mechanisms triggered by disparate antigens and their associated diseases. Furthermore, we demonstrated the possibility that PM2.5, malignancy, and gene expression specifically induce exposure of these antigens through conformational changes, molecular mimicry, or increased expression eliciting autoimmune responses. Thus, this review provides novel insights into the pathological mechanism of MN.

A risk association between membranous nephropathy (MN) and lung cancer is reported, but traditional observational studies cannot provide strong evidence of its causality. This study aimed to assess genome-wide association studies data for a causal relationship between MN and lung cancer using a two-sample Mendelian randomization (MR) approach. Inverse-variance weighted, and MR Egger regression techniques were used to determine the association of genetic variants from cohorts of MN and lung cancer patients. Independent genetic variants with genome-wide significance (P < 5×10^–8) were used to determine the direction of chance. Sensitivity analyses confirmed the accuracy of the results. The results suggest that MN is an exposure factor for lung cancer, validated using a second cohort of lung cancer patients (P < 0.001). There is insufficient evidence to suggest a causal relationship between lung cancer and MN; however, cigarette smoking may be a confounding factor for lung cancer due to MN. The findings provide causal evidence for the effect of MN on lung cancer risk and may be useful for patient management, especially in older patients with MN who should be systematically screened regularly.