Ask about this productRelated genes to: CKMM antibody
- Gene:
- CKM NIH gene
- Name:
- creatine kinase, M-type
- Previous symbol:
- CKMM
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-02-10
Related products to: CKMM antibody
Related articles to: CKMM antibody
- Cardiovascular-Kidney-Metabolic (CKM) syndrome represents a progressive cardiometabolic continuum. Whether the association between skeletal muscle health and cardiovascular risk is consistent across CKM stages remains unclear. - Source: PubMed
Publication date: 2026/08/23
Hou YingLu ZhenChi YongqianPei JixiangXu FengqiangDu ZhihangWang KuoJi HongweiGuo Junjie - This study seeks to explore the impact of lean and non-lean phenotypes of metabolic dysfunction-associated steatotic liver disease (MASLD) on the prevalence of advanced cardiovascular-kidney-metabolic (CKM) syndrome stage in individuals with type 2 diabetes mellitus (T2DM). - Source: PubMed
Publication date: 2026/08/07
Wang Jun-WeiJiang LeGao Lin-LinRen JieZhao Shi-YuQiao Ya-NanLiu Shi-Wei - Oxidative stress is a pathological driver of cardiovascular-kidney-metabolic (CKM) syndrome, exacerbating inflammation and tissue injury, while metabolic dysfunction-associated steatotic liver disease plays a central role in the progression of CKM. The Composite Dietary Antioxidant Index (CDAI), as a comprehensive measure of the overall antioxidant capacity of the diet, reflects an individual's exposure level to dietary antioxidants. This study aimed to evaluate the predictive value of CDAI combined with hepatic indices for disease progression and mortality risk in CKM patients. Data were derived from the US National Health and Nutrition Examination Survey 2001-2018. Using methods such as multivariate Cox regression analysis, survival analysis, mediation effect analysis, and machine learning, we examined the associations of CDAI and hepatic indices - including the Fatty Liver Index, NAFLD Fibrosis Score (NFS), AST to Platelet Ratio Index, and Fibrosis-4 Index (FIB-4) - with CKM staging and the risks of all-cause and cardiovascular disease (CVD) mortality among CKM participants. The fully adjusted model revealed that participants in the highest CDAI quartile had a significantly lower risk of all-cause mortality (hazard ratio = 0.717, 95% confidence intervals: 0.611-0.841; P < .0001) and CVD mortality (23.1% reduction) compared to the lowest quartile. Restricted cubic spline (RCS) analysis confirmed a significant inverse association between CDAI and both all-cause and CVD mortality. Elevated levels of hepatic indices were associated with increased all-cause and CVD mortality risk. Kaplan-Meier curve analysis also showed an inverse association between higher CDAI and all-cause/CVD mortality, whereas hepatic fibrosis indices (FIB-4, NFS, and AST to Platelet Ratio Index) were positively associated with mortality. Mediation analysis indicated that the protective effect of CDAI was independent of the liver fibrosis pathway but partially mediated through reduced hepatic steatosis. Furthermore, Light Gradient Boosting Machine demonstrated optimal performance in predicting advanced CKM stages. Advanced age, hepatic indices (NFS, FIB-4, and Fatty Liver Index), and vitamin E levels were key predictors of advanced CKM staging. Higher CDAI is associated with reduced all-cause and CVD mortality in CKM patients, while elevated hepatic indices correlate significantly with increased mortality risk. Both CDAI and hepatic indices serve as effective predictors for CKM risk stratification. - Source: PubMed
Yang ZhengSong ShupengLi Yongguo - Menopause is associated with unfavorable metabolic changes that may contribute to the development of metabolic dysfunction-associated steatotic liver disease (MASLD), chronic kidney disease (CKD), and increased cardiometabolic risk. Within the evolving cardiovascular-kidney-metabolic (CKM) framework, MASLD is increasingly recognized as a key driver rather than an outcome of metabolic dysfunction. The liver and kidneys closely interact to regulate metabolism, detoxification, ketogenesis, and endocrine signaling, which together influence whole-body metabolic homeostasis. Menopause and the menopausal transition may modify these interactions through alterations in body fat distribution, insulin sensitivity, inflammatory signaling, and hepatic and renal physiology, thereby contributing to disruption of the increasingly recognized liver-kidney-metabolic (LKM) axis. Advanced MASLD, owing to liver fibrosis, may further accelerate CKD through systemic insulin resistance, subclinical inflammation, gut dysbiosis, and accumulated nephrotoxic metabolites. Menopausal hormone therapy (MHT) may partially mitigate these alterations; however, its effects on the LKM axis are variable and context-dependent according to timing, formulation, route of administration, and baseline metabolic phenotype. Current evidence does not support the use of MHT for the prevention or treatment of MASLD or CKD, and treatment should be guided by established indications. Understanding menopause as a systems-level modifier of LKM health may therefore support more personalized preventive and therapeutic strategies targeting CKM health in peri- and postmenopausal women through a holistic and integrated approach. - Source: PubMed
Publication date: 2026/08/22
Jamalinia MohamadLonardo AmedeoWeiskirchen Ralf - Pancreatic resection is a profound physiologic stress test. Traditional risk assessment often focuses on procedure-specific technical failures, yet postoperative recovery depends heavily on a patient's systemic physiologic reserve. We evaluated the association between the American Heart Association's Cardiovascular-Kidney-Metabolic (CKM) syndrome framework and outcomes following pancreatic resection. - Source: PubMed
Publication date: 2026/08/20
Elgabsi MiriAbumouch IsisZilbermints VeacheslavBaker Fadi AbuHazzan RawiMahamid Ahmad