To analyze data indicating that type 2 diabetes mellitus (T2DM), atherosclerotic cardiovascular disease (ASCVD), heart failure with preserved ejection fraction (HFpEF), metabolic dysfunction-associated steatotic liver disease (MASLD), hypertension, and chronic kidney disease (CKD) arise along a unified cardiometabolic disease (UCD) continuum.
Approach:
Review Methodology: A structured narrative review was conducted using databases like PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar, focusing on mechanistic drivers and clinical endpoints.
Key Findings:
Visceral adipose tissue dysfunction and ectopic lipid accumulation are central to the UCD continuum, supported by mechanistic studies.
Stage-specific mediators such as ceramides, NLRP3, TMAO, and leptin-adiponectin ratio serve as biomarkers, as indicated by current evidence.
GLP-1 receptor agonists, SGLT2 inhibitors, and finerenone show benefits across multiple conditions, reflecting pharmacologic modulation of the continuum.
Interpretation:
The data support a UCD model where T2DM, ASCVD, MASLD, HFpEF, hypertension, and CKD are manifestations of a progressive pathophysiological continuum.
Limitations:
The review does not evaluate a single treatment or use the formal therapeutic GRADE method for evidence appraisal.
It does not address potential biases in the studies reviewed or the limitations of the available data.
Conclusion:
The proposed UCD continuum highlights mechanistic nodes amenable to biomarker development and therapeutic intervention.
