Ask about this productRelated genes to: CKMM protein
- 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 protein
Related articles to: CKMM protein
- This review examines the mechanistic, epidemiological and therapeutic evidence underpinning liver integration into the cardiovascular-kidney-metabolic (CKM) construct. For the purposes of this review, we use the term cardiovascular-renal-hepatic-metabolic (CRHM) syndrome to denote this expanded framework, acknowledging that consensus nomenclature is yet to be established. - Source: PubMed
Publication date: 2026/09/02
Marshall William RSinha SmeetaGreen DarrenKalra Philip A - Obesity and type 2 diabetes (T2D) are dominant drivers of chronic kidney disease (CKD) within the cardio-kidney-metabolic (CKM) syndrome. Despite advances with renin-angiotensin system inhibitors and sodium-glucose cotransporter 2 (SGLT2) inhibitors, substantial residual cardiovascular and renal risk persists, highlighting the need for therapies targeting upstream metabolic dysfunction. Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) have emerged as key modulators of CKM disease through integrated metabolic, vascular, and anti-inflammatory mechanisms. Cardiovascular outcome trials first established their cardioprotective effects, while the FLOW trial definitively demonstrated kidney protection, showing a 24% reduction in major kidney outcomes in patients with T2D and CKD. Mechanistic insights from translational studies further suggest that GLP-1 receptor activation promotes metabolic decongestion, improves intrarenal hemodynamics, and attenuates inflammatory and fibrotic pathways. Beyond selective GLP-1 receptor agonism, dual (glucose-dependent insulinotropic polypeptide [GIP]/GLP-1) and triple (GIP/GLP-1/glucagon) incretin agonists, including tirzepatide and retatrutide, extend this paradigm by delivering greater weight reduction and systemic metabolic reprogramming, with emerging signals for cardiovascular and renal benefit. Contemporary CKD management is shifting toward a phenotype-driven, layered therapeutic strategy in which SGLT2 inhibitors provide foundational kidney protection and incretin-based therapies are integrated to address residual metabolic and cardiovascular risk. In this evolving CKM framework, incretin-based therapies represent a central component of multi-mechanistic disease modification, extending beyond glycemic control to coordinated protection across the heart, kidney, and metabolic systems. - Source: PubMed
Publication date: 2026/09/01
Kim YaeniLee Eun Young - Advanced cardiovascular-kidney-metabolic (CKM) syndrome is highly prevalent. Diet is increasingly considered as a modifiable risk factor for advanced CKM syndrome. This study aims to evaluate the associations of B vitamin intakes with advanced CKM syndrome. - Source: PubMed
Publication date: 2026/08/17
Tu DingyuanLi JinruLuo LiWang Jianming - The associations of the triglyceride-glucose (TyG) index and its derived indices with the progression of cardiovascular-kidney-metabolic (CKM) syndrome remain poorly elucidated. - Source: PubMed
Publication date: 2026/08/17
An Jun-QiaoHe XueHao Qian-YingWu YanHe Qing-Yong - This study aims to evaluate the associations of Klemera-Doubal Method Biological Age Acceleration (KDM-BAA) and Phenotypic Age Acceleration (PAA) with all-cause and cause-specific mortality in U.S. adults with Cardio-Kidney-Metabolic (CKM) syndrome stages 0-3 and to establish risk prediction models. Data were obtained from 16,837 participants in NHANES 1999-2010 and 2015-2018, linked to mortality through 2019. Biological age was estimated using KDM-BA and Phenotypic Age algorithms, with residuals defining Biological Age Acceleration (BAA). Cox proportional hazards models were applied, and LASSO-Cox nomograms were developed for mortality prediction. Over a median follow-up of 11.33 years, 10.8% of the weighted population (9.75 million adults) died. After full adjustment for confounders, KDM-BAA positivity increased the risk of all-cause, CVD, and non-CVD mortality by 41%, 74%, and 31%, respectively; PAA positivity showed even larger increases - 103%, 79%, and 112%. Both metrics consistently exhibited a positive association in multiple subgroups and sensitivity analyses. The LASSO-Cox-based nomogram showed favorable discrimination (training AUCs 0.776 and 0.775 at 10 and 20 years; validation AUCs 0.765 and 0.757, respectively) and good calibration, suggesting potential clinical applicability. BAA independently predicts long-term mortality among individuals with CKM stages 0-3. PAA provides superior prognostic value, supporting the importance of monitoring biological aging to guide early intervention and improve long-term outcomes. - Source: PubMed
Chen XiaoqiangHuang YisenHuang YingxuanLi YingyiChen XinqiWang YubinLiu Xiaoqiang