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
- BACKGROUND Despite the well-established epidemiological association between diabetic kidney disease (DKD) and coronary artery disease (CAD) in patients with T2DM, which reflects a core feature of cardiovascular-kidney-metabolic (CKM) syndrome, the underlying molecular mechanisms connecting these 2 conditions remain unclear. Within this integrated pathophysiological framework, the potential role of lipocalin-2 (LCN2) was investigated. MATERIAL AND METHODS A total of 917 participants with T2DM were stratified into an overall cohort and a BMI-, age-, and sex-matched sub-cohort. Serum LCN2 levels were measured. Immunohistochemistry was performed on cardiac and renal tissues from high-fat diet/streptozotocin-induced diabetic mice. Renal tubular (HK-2) and cardiomyocyte (H9c2) cells were treated with recombinant LCN2 to assess inflammatory responses. RESULTS DKD severity was identified as an independent risk factor for CAD in patients with T2DM. Serum LCN2 levels were significantly elevated in patients with DKD or CAD, and were closely correlated with DKD severity and B-type natriuretic peptide levels. Logistic regression analysis further indicated that an elevated serum LCN2 level served as an independent risk factor for the presence of DKD or CAD. Importantly, mediation analysis revealed that increased serum LCN2 may partially mediate the bidirectional association between DKD and CAD. Consistent with these clinical findings, animal experiments demonstrated concurrent upregulation of LCN2 in both the heart and kidney tissues of diabetic mice. Recombinant LCN2 dose-dependently increased interleukin-6 and tumor necrosis factor-a mRNA expression in HK-2 and H9c2 cells. CONCLUSIONS LCN2 may represent a potential biomarker and partial mediator between DKD and CAD in T2DM, potentially contributing to CKM-related organ crosstalk. - Source: PubMed
Publication date: 2026/08/16
Huang XinmeiWu YueyueWang LihongJia JunjieWu TianyiLiu WenjuanWang YiFan YeyaoGong WeiZhang LiLiu JunZang ShufeiZhang Zhaoyun - Cardiovascular-kidney-metabolic (CKM) syndrome spans stages 0-4, with stage 4 denoting clinical cardiovascular disease (CVD). While individuals in stages 0-3 face elevated incident CVD risk, how different durations of physical activity (PA) associate with this risk remains unclear. - Source: PubMed
Publication date: 2026/07/31
An Jun-QiaoHe XueDing Jing-YiWu YanLuan Xiang-WeiXu Zhao-ZongGuo Tian-TianHe Qing-Yong - IntroductionCardiovascular-kidney-metabolic (CKM) syndrome is characterized by chronic inflammation that may drive heart failure. Peritoneal dialysis (PD), while lifesaving, may induce local and systemic inflammation through bioincompatible intraperitoneal solutions, potentially amplifying CKM syndrome. We investigated peritoneal mononuclear phagocyte phenotypes, key-drivers of inflammation, and whether these correlate with systemic inflammation and cardiac function in PD-treated patients.MethodsWe collected patient-matched peripheral blood-derived and PD-effluent (PDE)-derived cells from 13 adult PD-treated patients and characterized peritoneal immune populations by unbiased clustering using a mononuclear phagocyte-selective flow cytometry panel. In a subsequent cohort of 21 PD-treated patients, we correlated cardiac function [left ventricular global longitudinal strain (LV-GLS)] with peritoneal immune profiles and serum inflammatory markers.ResultsMononuclear phagocytes predominated in PDE and exhibited a more differentiated phenotype than blood-derived mononuclear phagocytes. Unbiased clustering revealed substantial overlap between blood- and PDE-derived classical monocytes. A higher PDE-derived differentiated monocyte-to-dendritic cell ratio was related to more impaired LV-GLS. Peritoneal monocytes showed reduced antigen-presenting capacity in patients with impaired cardiac function, potentially influenced by diabetes mellitus. Systemic inflammatory markers were largely undetectable in this stable PD-cohort.ConclusionOur findings suggest a link between peritoneal immune characteristics and cardiac dysfunction, characterized by a shift towards a higher monocyte-to-dendritic cell ratio in PD-treated patients with more pronounced cardiac dysfunction. The directionality and mechanisms underlying this association remain to be established and given the limited patient number and cross-sectional design, these findings should be considered as hypothesis-generating. The applied flow cytometry and unsupervised clustering approach offers a promising and scalable tool for future in-depth investigation of the peritoneal immune microenvironment and its relation to PD-related clinical outcomes, including CKM sequelae. - Source: PubMed
Publication date: 2026/08/14
Karsten MickyHahn NicoVree PuckDavies Luke CVervloet Marc GVan Den Bossche JanJakulj Lily - Recently, the American Heart Association defined, staged, and highlighted the multisystem consequences of poor cardiovascular-kidney-metabolic (CKM) syndrome health with a clarion call to harmonize guidelines and provide opportunities for actionable preventive interventions before overt CVD. In the United States, the components that comprise CKM (obesity, diabetes, hypertension, etc.) are potent risk factors for poor maternal and neonatal outcomes, with a disproportionate burden among racial/ethnic minorities. However, population-level data on CKM syndrome in reproductive-aged women are scarce, but a critical prerequisite in evaluating the impact of CKM stages on overall pregnancy outcomes. - Source: PubMed
Publication date: 2026/02/17
Broni Eric KAryee Ebenezer KLachaud AmberPeprah AmponsahLewey JenniferLevine Lisa D - To evaluate the role of finerenone, a nonsteroidal mineralocorticoid receptor antagonist (MRA), in heart failure with preserved or mildly reduced ejection fraction (HFpEF/HFmrEF). - Source: PubMed
Publication date: 2026/08/13
Khidhir AngelaKalra Dinesh K