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April 15, 2026Journal of DiabetesOpen Access

Genomic SEM identifies 32 novel loci for CKM syndrome, localizing signals to pancreatic islet cells.

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Why the study?

The genetic basis of cardiovascular-kidney-metabolic syndrome involves complex pleiotropy, requiring analytical approaches able to dissect shared genetic architectures across multiple cardiometabolic traits.

Population

Summary statistics from six cardiometabolic traits and 1,862,425 SNPs

Design

Genomic structural equation modeling and genome-wide association analyses

Key result

Genomic structural equation modeling identified 2,212 significantly associated variants and 32 novel loci for cardiovascular-kidney-metabolic syndrome, localizing signals to pancreatic islet cells.

Authors

CLChuanlong LuLLLizheng LiJCJinshan Chen

Discussion

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Overview

Should not yet change practice in CKM syndrome; extends shared genetic architecture with links to pancreatic islet regulation.

Key Points

  • This research aims to explore the genetic architecture of cardiovascular-kidney-metabolic syndrome using advanced genomic modeling techniques.
  • Utilized genomic structural equation modeling to analyze six cardiometabolic traits.
  • Conducted genome-wide association analyses on 1,862,425 SNPs.
  • Applied LD Score regression to evaluate polygenic heritability and confounding bias.
  • Identified novel loci using GWAS-by-Subtraction and performed functional characterization through TWAS and pathway enrichment analysis.
  • Achieved excellent model fit (CFI = 0.99) indicating robustness of findings.
  • Identified 2,212 significant variants and discovered 32 novel loci associated with CKMs.
  • TWAS highlighted 188 high-confidence genes with SENP2 and KIF11 showing the strongest positive associations.
  • Pathway enrichment implicated lipid balance and proteolysis, specifically in pancreatic islet cells.

Study Design

Type

Observational

Structured PICO

P
Population
Summary statistics from six cardiometabolic traits analyzing 1,862,425 SNPs
I
Intervention
Genomic structural equation modeling (genomic SEM) and GWAS-by-Subtraction
O
Outcome
Identification of shared genetic architectures, novel risk loci, and pathogenic mechanisms across multiple cardiometabolic traitssurrogate

This study reveals the shared genetic architecture of cardiovascular-kidney-metabolic syndrome, identifying novel risk loci and establishing a cellular link to endocrine metabolic regulation in pancreatic islets.

Cite This Study

Lu et al. (2026) conducted an observational in Cardiovascular-kidney-metabolic syndrome (CKMs). Genomic structural equation modeling was evaluated on Significantly associated variants and novel loci for CKMs. Genomic structural equation modeling identified 2,212 significantly associated variants and 32 novel loci for cardiovascular-kidney-metabolic syndrome, localizing signals to pancreatic islet cells.

synapsesocial.com/papers/69df2c1de4eeef8a2a6b1222https://doi.org/10.1111/1753-0407.70225
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Genomic structural equation modelling provides insights into the shared multivariate genetic architecture of cardio-kidney-metabolic syndrome components2025
  2. 2Integrative genomic dissection of cardio-kidney-metabolic syndrome reveals novel loci, causal genes, and tissue-specific pathways in European populations2026
  3. 3Cardiovascular-kidney-metabolic syndrome: candidate subtypes and genetic risk factors2026 · 1 citations
  4. 4Metabolic-Renal Disease Genetics Architecture Revealed by Genomic Structural Equation Modeling2026
  5. 5Cardio-Kidney-Metabolic Syndrome: Candidate Subtypes and Genetic Risk Factors2025