{"title":"Exploring the potential targets and molecular mechanisms of cordycepin against gastric cancer based on bioinformatics analysis and network pharmacology.","authors":"Zijing Huang, Shuiqing Li, Yan Zhang","doi":"10.3164/jcbn.25-276","DOIUrl":"10.3164/jcbn.25-276","url":null,"abstract":"<p><p>This study aimed to investigate the molecular targets and anti-tumor mechanisms of cordycepin in gastric cancer (GC). Bioinformatics analysis was performed using the GSE65801 dataset to identify differentially expressed genes (DEGs) in GC. Potential cordycepin targets were screened from the CTD database, and the key gene was identified by intersecting these targets with GC DEGs and constructing a PPI network. The expression of fibronectin 1 (FN1) in GC was validated using public databases (TIMER, GEPIA, and UALCAN) and <i>in vitro</i> experiments in GC cell lines (AGS and HGC-27). The functional effects of cordycepin, alone or in combination with FN1 overexpression, on cell proliferation (CCK8 and colony formation assay), apoptosis (flow cytometry), and the PI3K/AKT pathway (Western blot) were assessed. A total of 649 DEGs were identified in GC and 336 potential targets of cordycepin were screened. FN1 was screened as a key intersection target of cordycepin and GC, and was found to be significantly upregulated in GC tissues and cells. High FN1 expression was associated with poor patient survival. Cordycepin treatment significantly inhibited the viability of GC cells and downregulated FN1 protein expression. Functionally, cordycepin suppressed cell proliferation and induced apoptosis by the inhibition of the PI3K/AKT pathway, and these effects were reversed by overexpression of FN1. In conclusion, cordycepin inhibited GC cell growth partially through the downregulation of FN1 and inactivation of the PI3K/AKT pathway, suggesting that FN1 was a novel potential target for cordycepin in the treatment of GC.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"131-140"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypoglycemia and altered bile acid metabolism are linked to latent iron deficiency in young Japanese women.","authors":"Sena Ishikawa, Rika Miyazawa, Fumika Yokoyama, Daisuke Sawamura, Sandra Iuliano-Burns, Kei-Ichi Nakajima, Satoshi Ishizuka","doi":"10.3164/jcbn.25-279","DOIUrl":"10.3164/jcbn.25-279","url":null,"abstract":"<p><p>Iron deficiency anemia (IDA) remains a prevalent health issue, especially among Japanese women, and may be influenced by dietary patterns and lipid metabolism. This study aimed to investigate the association between circulating bile acid (BA) concentrations and iron-related biomarkers in young Japanese women. Blood biochemical and anthropometric data were collected from 33 healthy young women aged 20. The participants can be divided into two groups based on the levels of total-iron binding capacity (TIBC), although their hemoglobin and ferritin levels were in the normal ranges. When participants were divided based on TIBC, the low TIBC group showed significantly higher levels of 12-hydroxylated, non-12-hydroxylated, and total BAs, as well as significantly lower blood glucose levels compared to the normal group (<i>p</i><0.05). Positive correlations were observed between TIBC and specific BA species, such as glycolithocholic acid (<i>ρ</i> = 0.3993, <i>p</i><0.0288), cholic acid (<i>ρ</i> = 0.4767, <i>p</i><0.0077), and taurocholic acid (<i>ρ</i> = 0.4423, <i>p</i><0.0144). Additionally, transferrin levels were positively correlated with glycolithocholic acid (<i>ρ</i> = 0.3649, <i>p</i><0.0474). These findings suggest that TIBC may serve as an early indicator of hypoglycemia, reflecting preclinical metabolic disturbance, in addition to being a latent IDA marker.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"158-162"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comparative neuroprotective and antioxidant roles of vitamin E isoforms: a review.","authors":"Liu Yuhong, Koji Fukui","doi":"10.3164/jcbn.26-93","DOIUrl":"10.3164/jcbn.26-93","url":null,"abstract":"<p><p>Vitamin E comprises eight structurally related isoforms, including α-, β-, γ-, and δ-tocopherols and their corresponding tocotrienols. These isoforms differ in the degree of methylation of the chromanol ring and the saturation of the side chain, structural features that critically influence their bioavailability, antioxidant capacity, and neuroprotective functions. This mini review systematically summarizes recent advances in the antioxidant and neuroprotective roles of vitamin E isoforms, with particular emphasis on their distinct mechanisms of action in the nervous system. Evidence from cell-based studies, animal models, and human investigations indicates that the neuroprotective effects of vitamin E isoforms vary considerably. Tocotrienols, characterized by their unsaturated side chains, exhibit enhanced membrane mobility and broader biological activity, demonstrating superior neuroprotective properties through modulation of signaling pathways, maintenance of mitochondrial function, and inhibition of abnormal tau hyperphosphorylation. In addition, different tocopherol isoforms show complementary roles in scavenging reactive oxygen species and/or reactive nitrogen species. Despite substantial experimental evidence, clinical data remain limited, and challenges such as differences in bioavailability and incomplete understanding of isoform-specific mechanisms persist. Overall, vitamin E should be regarded not as a single molecule but as a family of functionally complementary isoforms, whose synergistic actions may play a crucial role in maintaining brain health and in the prevention and treatment of neurodegenerative diseases.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"125-130"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557795/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Combined inhibition of MEK and FOXO1 synergistically suppresses MDA-MB-231 cell proliferation with reduced LOXL4.","authors":"Tetsuro Kamiya, Asumi Kanaya, Tomohiro Otsuka, Hirokazu Hara","doi":"10.3164/jcbn.26-55","DOIUrl":"10.3164/jcbn.26-55","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is characterized by its aggressive phenotype and limited therapeutic options. FOXO1, a member of the O-class of forkhead transcription factors, has been implicated in various oncogenic processes, yet its specific role in TNBC remains to be fully elucidated. This study aimed to investigate the effects of the FOXO1-selective inhibitor, AS1842856, on the proliferation of the human TNBC cell line MDA-MB-231 and to identify the underlying molecular mechanisms. Treatment with AS1842856 significantly suppressed the proliferation of MDA-MB-231 cells in a dose-dependent manner. Additionally, AS1842856 suppressed the expression of lysyl oxidase-like 4 (LOXL4). Given LOXL4 is known to be involved in extracellular matrix remodeling and is frequently associated with cancer progression and metastasis, AS8142856 has been considered to suppress MDA-MB-231 cell migration. Interestingly, however, the knockdown of FOXO1 did not lead to a significant reduction in LOXL4 expression levels, suggesting that AS1842856 suppresses LOXL4 expression through FOXO1-independent mechanisms. We found that AS1842856-mediated ERK activation and intracellular reactive oxygen species are crucial in reducing LOXL4. Furthermore, the combined action of pharmacological inhibition of ERK pathways and AS1842856 suppressed MDA-MB-231 cell migration. These findings demonstrate that the ERK-LOXL4 signaling axis may play a critical role in the proliferation of TNBC cells. In conclusion, targeting the LOXL4 and ERK pathways pharmacologically could provide a novel therapeutic strategy for the treatment of aggressive breast cancers.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"150-157"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chemical generation of superoxide in the co-presence of riboflavin derivatives and NADH: evidence for a non-enzymatic redox pathway.","authors":"Rinka Sugita, Sayaka Iida, Midori Nagase, Hitoshi Masaki, Yorihiro Yamamoto, Akio Fujisawa","doi":"10.3164/jcbn.26-99","DOIUrl":"10.3164/jcbn.26-99","url":null,"abstract":"<p><p>We recently reported that flavin-associated compounds such as riboflavin, flavin mononucleotide, and flavin adenine dinucleotide reduce oxidized coenzyme Q and vitamin K homologues to corresponding reduced forms in the presence of reduced β-nicotinamide adenine dinucleotide (NADH). In these processes, coenzyme Q or vitamin K acts as a terminal electron accepter. If oxygen can function as an electron acceptor instead of those quinones, resulting in the formation of superoxide. In this study, superoxide formation from the system of NADH and flavin-associated compounds was examined using a water-soluble tetrazolium salt (WST-1) and 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazin-3-one (MCLA) assays. Formation of WST-1 formazan and chemiluminescence from MCLA, both of which are specific to superoxide, increased during co-incubation with NADH and a flavin-associated compound, and significantly suppressed with the addition of superoxide dismutase (SOD). Superoxide is an important reactive oxygen species (ROS) that is converted to other ROS, such as hydrogen peroxide or peroxynitrite. HaCaT keratinocytes, immortalized human keratinocytes, were then cultivated with NADH and flavin-associated compounds. Cell viability declined with increasing NADH concentration but was significantly recovered following the addition of SOD and catalase. We propose a chemical pathway for flavin-associated compound and NADH-induced superoxide generation <i>in vivo</i>, in which extracellular SOD plays an important role in cell survival.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"163-169"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Organ-specific modulation of antioxidant functions by combined voluntary exercise and radon inhalation in mice.","authors":"Reiju Takenaka, Ayumi Tanaka, Shogo Miyanaga, Shota Naoe, Shuna Goto, Mitsuki Nagano, Kotaro Tano, Norie Kanzaki, Akihiro Sakoda, Kiyonori Yamaoka, Takahiro Kataoka","doi":"10.3164/jcbn.26-46","DOIUrl":"10.3164/jcbn.26-46","url":null,"abstract":"<p><p>Radon inhalation as well as voluntary exercise increase antioxidant function in experimental animals. However, the combined effects of radon inhalation and exercise on antioxidant functions have not yet been investigated. In this study, we examined the effects of combined voluntary wheel running (VWR) and radon inhalation on antioxidant functions in various organs of mice. Mice were individually housed in cages equipped with running wheels, and allowed voluntary exercise for 5, 15, or 25 days, followed by radon inhalation at 2,000 Bq/m<sup>3</sup> for 24 h. Antioxidant function was enhanced by the combined treatment in the kidneys, pancreas, spleen, and stomach, with responses varying according to exercise duration. In contrast, antioxidant function was reduced in the lungs and heart. No clear interaction effects of the combined treatment were observed in the liver, small intestine, colon, and brain. These findings suggest that the combined effects of voluntary exercise and radon inhalation on antioxidant functions are organ-specific and can be categorized into distinct response patterns across tissues.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 2","pages":"141-149"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Haixia Huang, Yahong Zhou, Jing Hu, Fan Jia, Yong Tan
{"title":"The mechanism of polycystic ovarian syndrome induced by circadian rhythm disturbance and the therapeutic effect of melatonin.","authors":"Haixia Huang, Yahong Zhou, Jing Hu, Fan Jia, Yong Tan","doi":"10.3164/jcbn.25-255","DOIUrl":"10.3164/jcbn.25-255","url":null,"abstract":"<p><p>Environmental factors are crucial causes of polycystic ovary syndrome (PCOS). There is growing evidence of an association between circadian rhythm disturbance and PCOS, but the underlying molecular mechanisms This study aimed to explore the molecular mechanism of PCOS induced by circadian rhythm disturbance and evaluate the therapeutic potential of melatonin. A rat model of circadian rhythm disturbance was established via 24-h continuous light exposure. Rats were randomly divided into the Control group (normal circadian rhythm), Model group (continuous light exposure), and Model + Melatonin treatment group (continuous light exposure + melatonin). Reproductive endocrine indicators, ovarian histomorphology, and ovarian granulosa cell (GC) function were assessed. Additionally, circadian rhythms of serum hormones, autophagy-related markers (LC3), and hypothalamic clock genes were detected at six zeitgeber time (ZT) points. Autophagy and apoptosis levels in GCs, as well as the activation of MAPK and PI3K/Akt/mTOR pathways, were also detected. Continuous light exposure induced PCOS-like phenotypes in rats, characterized by disrupted estrous cycles, cystic ovarian changes, and loss of circadian rhythms in serum hormones, autophagy marker LC3, and hypothalamic clock genes. Moreover, continuous light exposure reduced GC viability, increased GC autophagy and apoptosis, activated the MAPK pathway, and inhibited the PI3K/Akt/mTOR pathway in GCs. Melatonin treatment significantly ameliorated these PCOS-like phenotypes. Our study showed circadian rhythm disturbance induced PCOS via MAPKs and PI3K/Akt/mTOR signaling pathways and increased autophagy level in rat ovarian GCs. Melatonin had a therapeutic effect on PCOS by reversing these signaling pathway abnormalities and reducing autophagy and apoptosis levels in GCs.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 1","pages":"76-85"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anti-aging effects of glycyrrhizin via maintaining Klotho levels.","authors":"Shiho Ohnishi, Keiichi Hiramoto, Nobuji Yoshikawa, Shosuke Kawanishi","doi":"10.3164/jcbn.25-263","DOIUrl":"10.3164/jcbn.25-263","url":null,"abstract":"<p><p>Klotho, an anti-aging protein, controls the insulin-like growth factor-1 (IGF-1) and suppresses inflammation implicated in senescence. We previously reported that glycyrrhizin (GL), a medicinal ingredient of licorice root, significantly attenuates inflammatory responses by inhibiting high-mobility group box 1 (HMGB1). In this study, we investigated whether GL is effective in suppressing the decline in Klotho levels and aging-induced frailty. After oral administration of GL three times a week for 12 months, the following effects were observed: reductions in the increases in blood fats, steatoses, obesity, and kidney aging; maintenance of activity level and rotarod test performance. Furthermore, we found beneficial effects of GL on the blood levels of functional proteins; upregulation of anti-aging factors, IGF-1 and Klotho; decrease in cystatin-C, an indicator of declining kidney function; and decreases in IL-6 and TNF-α, inflammatory cytokines. GL also seemed to increase superoxide dismutase 2, an antioxidant enzyme, in the liver and kidneys. As GL can inhibit HMGB1, it may attenuate this inflammatory amplification loop, reducing the systemic senescence-associated secretory phenotype and thus mitigating multiple aging phenotypes by maintaining Klotho levels.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 1","pages":"104-110"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic potential of hydrogen-rich water (HRW) in oxidative stress-related diseases.","authors":"Wafaa H Mohamed, Idris Long","doi":"10.3164/jcbn.26-5","DOIUrl":"10.3164/jcbn.26-5","url":null,"abstract":"<p><p>Oxidative stress is a central mechanism in metabolic, cardiovascular, and neurodegenerative diseases, contributing to inflammation, mitochondrial dysfunction, and apoptosis. Consequently, redox-modulating therapies are increasingly explored as potential therapeutic strategies. This review evaluates the mechanistic basis, experimental evidence, and clinical applicability of hydrogen-rich water (HRW) in oxidative stress-related diseases. A structured literature search identified mechanistic, preclinical, and clinical studies investigating HRW or molecular hydrogen (H<sub>2</sub>) on oxidative stress, inflammation, mitochondrial regulation, and disease-related outcomes. Due to substantial methodological heterogeneity, findings were synthesized qualitatively. HRW has been proposed to selectively neutralize highly reactive species such as hydroxyl radicals (<sup>•</sup>OH) and peroxynitrite (ONOO<sup>-</sup>) while preserving physiological reactive oxygen species signalling. Mechanistic studies demonstrate activation of nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) pathways, suppression of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) inflammatory cascades, modulation of JAK/STAT signalling, preservation of mitochondrial bioenergetics, and enhancement of autophagic regulation. Preclinical and clinical studies report improvements in glycaemic control, endothelial function, cardiometabolic health, neuroprotection, exercise performance, and treatment-related fatigue. Despite an excellent safety profile, standardization of HRW preparation and large multicentre randomized controlled trials (RCTs) remain necessary to establish clinical efficacy and translational potential.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 1","pages":"15-27"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impact of nine dietary minerals on the risk of chronic kidney disease: a multi-model analysis in US adults using NHANES data.","authors":"Zhuoga Cairen, Xinyun Chen, Shenju Gou, Ping Fu","doi":"10.3164/jcbn.25-251","DOIUrl":"10.3164/jcbn.25-251","url":null,"abstract":"<p><p>Chronic kidney disease (CKD), affecting 8-16% of the global population, presents substantial public health burdens. While constituting only 5% of daily dietary intake, minerals critically influence physiological processes. This study investigates associations between dietary mineral intake and CKD risk; utilizing publicly available data from the National Health and Nutrition Examination Survey (NHANES), we employed multivariate logistic regression, restricted cubic spline (RCS), weighted quantile sum (WQS), quantile-based g-computation (QGcomp), and Bayesian kernel machine regression (BKMR) models to assess CKD-mineral relationships; multivariate logistic regression revealed significant inverse associations between CKD risk and calcium (OR = 0.72), phosphorus (OR = 0.69), magnesium (OR = 0.65), copper (OR = 0.81), potassium (OR = 0.85), and zinc (OR = 0.88). RCS analysis demonstrated linear protective trends for calcium, phosphorus, zinc, potassium, and selenium, while magnesium, iron, and copper exhibited U-shaped dose-response patterns. WQS regression identified a protective mineral mixture (weighted index OR = 0.83), with magnesium (35.2%) and calcium (28.1%) as primary contributors. QGcomp analysis highlighted magnesium's protective effect (-0.21 risk score) contrasting with iron's adverse association (+0.18). BKMR modeling confirmed magnesium's significant protection (PIP = 0.92) and sodium's risk elevation (PIP = 0.87); magnesium and calcium emerge as robust protective factors against CKD, while sodium intake increases disease risk. Phosphorus, potassium, zinc, and copper demonstrate potential benefits, whereas iron shows context-dependent effects. These findings emphasize mineral-specific dietary strategies for CKD prevention.</p>","PeriodicalId":15429,"journal":{"name":"Journal of Clinical Biochemistry and Nutrition","volume":"79 1","pages":"60-68"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13412478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}