Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the kidneys. A concerted, increased FFA uptake due to high fat diets, overexpression of fatty acid uptake systems such as the CD36 scavenger receptor and the fatty acid transport proteins, and a reduced β-oxidation rate underlie the intracellular lipid accumulation in non-adipose tissues. FFAs in excess can damage podocytes, proximal tubular epithelial cells and the tubulointerstitial tissue through various mechanisms, in particular by boosting the production of reactive oxygen species (ROS) and lipid peroxidation, promoting mitochondrial damage and tissue inflammation, which result in glomerular and tubular lesions. Not all lipids are bad for the kidneys: polyunsaturated fatty acids (PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) seem to help lag the progression of chronic kidney disease (CKD). Lifestyle interventions, especially dietary adjustments, and lipid-lowering drugs can contribute to improve the clinical outcome of patients with CKD.

In traditional Chinese medicine (TCM), type 2 diabetes mellitus (T2DM) is regarded as Xiao Ke disease. Liuwei Dihuang pills (LWP), a classical TCM formula, with the function of nourishing kidney yin, has been used for treating Xiao Ke disease in clinic. In this review, we systematically highlighted recent evidence on LWP and T2DM data from clinical and animal studies, summarized the clinical application, pharmacological mechanism and the active compounds of LWP for the treatment of T2DM. This systematic review will provide an insightful understanding of TCM formulas, pharmacological mechanisms, medicinal-disease interactions, and will lay a foundation for the development of new drug therapy for T2DM.

Inflammatory bowel disease (IBD) is a chronic, immune-mediated intestinal disorder driven by dysregulated immune responses in genetically susceptible individuals. Despite recent advances in treatment, more than 30% of patients either fail to respond initially or lose response over time, underscoring the need for a deeper mechanistic understanding of immunogenetic pathways and the development of individualized therapeutic strategies. We first discuss how newly identified susceptibility genes (e.g., IL23R, NOD2, BDNF, SLC) and their polymorphisms influence immune cell function and epithelial barrier integrity. Single-cell technologies have further revealed novel cell subsets and interactions underlying disease heterogeneity. We then explore the clinical efficacy of classical and emerging targeted therapies, including cytokine-specific biologics, JAK inhibitors, and novel strategies aimed at restoring regulatory T-cell function or blocking integrin-mediated lymphocyte trafficking. Additionally, we highlight promising therapeutic approaches such as fecal microbiota transplantation, microbial metabolite-based interventions, and nanotherapeutics. We further discuss how genetic insights and immune biomarkers can facilitate treatment personalization and improve prognostic stratification. Ultimately, this review emphasizes the transition from broad immunosuppression to precision medicine and proposes integrated approaches—combining multiomics profiling, immune monitoring, and novel therapeutics—to achieve sustained remission and improve long-term outcomes in IBD patients.

This study was aimed at determining the antimetastatic effect of polyphyllin II (PPII) in bladder cancer (BC) and the underlying mechanisms in vitro and in vivo. Wound healing, Transwell assays, and phalloidin staining were performed to determine the effects of PPII on BC cell migration, invasion, and cytoskeletal formation. Gene transcription and expression changes were detected via RNA sequencing and western blotting. The subchronic toxicity and antimetastatic effects of PPII were evaluated in Nu/Nu nude mice. PPII inhibited the migration and invasion of BC cells. Bioinformatics analysis indicated that cytoskeletal regulation was a potentially regulated process. PPII restrained cytoskeletal formation, as confirmed by phalloidin staining. Mechanistically, PPII was found to decrease p-LIMK1/2 and p-CFL1 expression through ROCK1, and to inhibit increased p-CFL1 levels and invasion and migration abilities of BC cells induced by constitutively active RHOA. Subchronic toxicity evaluation revealed that 3.0 mg/kg PPII had limited effects on tissue morphology, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase. Furthermore, PPII treatment effectively inhibited the formation of pulmonary metastatic nodules, as well as the expression of ROCK1, p-LIMK1, and p-CFL1 in the lungs. Thus, PPII inhibits BC cell invasion, migration, and metastasis through the RHOA-ROCK1-LIMK1/2-CFL1 axis, and is a potential candidate for antimetastatic drug development.