Kidney diseases, characterized by renal dysfunction, are among the leading causes of death worldwide. Preventing and treating kidney diseases is important for reducing their associated morbidity and mortality. Moderate physical exercise has been recognized to be advantageous for kidney health. Irisin is an exercise-induced myokine identified in 2012. It plays an important role in energy and bone metabolism, oxidative stress reduction, anti-inflammatory processes, prevention of cell death, and cardiovascular protection. However, the relationship between irisin and kidney disease has not been fully elucidated. This review explores the role of irisin as a biomarker in the diagnosis of kidney diseases and their associated complications, elucidating the mechanisms through which it participates in various cell death pathways, such as apoptosis, autophagy, pyroptosis and ferroptosis. Furthermore, the levles of irisin secretion are discussed to provide a basis for the preventing and treating kidney diseases, as well as therapeutic guidance for developing new and promising intervention strategies.

Objective: The effects of green tea on metabolic diseases such as obesity and diabetes have been extensively studied. Obesity often leads to insulin resistance, particularly in peripheral tissues such as skeletal muscle. Green tea has shown promise in mitigating insulin resistance in several diet-induced obesity models. However, its ability to improve insulin sensitivity by modulating skeletal muscle metabolism in the absence of metabolic stress, such as constant cold exposure, remains unclear. Therefore, the aim of this study was to evaluate the effect of green tea on skeletal muscle metabolism in high-fat diet (HFD)-induced obese mice maintained at thermoneutrality (28°C). Methods: Male C57BL/6 mice were fed a control diet or a HFD for four weeks. Then, the HFD group mice were treated with green tea extract (500 mg/kg of body weight) while maintained at thermoneutrality (28°C). At the end of the experimental protocol, we performed metabolic analyses. Results: This study suggested that green tea treatment attenuates the negative effects of HFD by improving muscle muscle fiber cross-sectional area (CSA) in the gastrocnemius muscle and increasing the expression of genes involved in lipid metabolism. Although no effect was observed on fatty acid oxidation, green tea improved insulin and glucose sensitivity, as evidenced by glucose and insulin tolerance tests. It also increased the expression of genes associated with glucose uptake and lactate dehydrogenase activity in skeletal muscle. Conclusion: These findings suggest that green tea treatment improves insulin sensitivity by influencing skeletal muscle metabolism even in obese mice maintained at thermoneutrality.

Lung adenocarcinoma (LUAD) represents the predominant subtype of non-small cell lung cancer, with limited survival improvements despite advances in targeted therapies, underscoring the need for novel biomarkers and therapeutic targets. Apolipoprotein A1 (APOA1), a major component of high-density lipoprotein involved in cholesterol transport, has been linked to tumorigenesis. However, its role in LUAD remains unclear. Multi-omics analyses were conducted using TCGA, HPA, UALCAN, cBioPortal, and other databases to assess APOA1 expression, mutations, epigenetic modifications, prognostic correlations, immune infiltration via CIBERSORT, and pathway enrichment through GO, KEGG, and GSEA. We analyzed TCGA transcriptomic data to assess APOA1 expression in pan-cancer contexts, focusing on LUAD. Serum APOA1 levels were quantified by ELISA in 60 LUAD patients and 30 healthy controls. In vitro experiments involved APOA1 overexpression in A549 and SPCA1 cell lines, evaluated by Western blot, CCK-8 proliferation assay, and Transwell assays. In vivo tumor growth was assessed in nude mouse xenografts. APOA family genes predominantly exhibit amplifications and mutations in pan-cancer. APOA1 was significantly downregulated in LUAD tissues and serum, correlating with poor overall survival (AUC=0.942 for diagnostic accuracy). APOA1 modulates immunity and pathways like complement cascades. Overexpression inhibited cell proliferation, migration, and invasion in vitro, and reduced xenograft tumor volumes in vivo. Drug sensitivity analysis revealed enhanced efficacy of agents like selumetinib in high-APOA1. These findings position APOA1 as a tumor suppressor and prognostic biomarker in LUAD, offering potential for targeted therapies to improve patient outcomes.