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Related Experiment Videos

A Cross-Layer Inflammatory Signature Links Residual Inflammatory Risk to Heart Failure Risk in Metabolic Syndrome:

Chunmei Chen1,2, Xinxin Mao1,2, Yuxin Wang1,2

  • 1Department of General Internal Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.

Journal of Inflammation Research
|July 15, 2026
PubMed
Summary

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Residual inflammatory risk (RIR) is linked to increased heart failure (HF) risk in metabolic syndrome (MetS). This association is supported by shared inflammatory pathways and gene signatures across clinical and experimental models.

Area of Science:

  • Cardiovascular Medicine
  • Metabolic Disorders
  • Inflammation Biology

Background:

  • Residual inflammatory risk (RIR), often measured by high-sensitivity C-reactive protein (hs-CRP), signifies ongoing inflammation not fully addressed by standard metabolic markers.
  • The relationship between RIR and an elevated heart failure (HF) risk phenotype within metabolic syndrome (MetS), and its underlying inflammatory signature, requires further elucidation.

Purpose of the Study:

  • To investigate the association between RIR and a heightened HF-risk phenotype in patients with MetS.
  • To characterize the inflammatory signatures related to this association across clinical, bioinformatic, and experimental data.

Main Methods:

  • Utilized a propensity score-matched cohort of MetS patients to assess RIR's link to HF risk.
  • Integrated gene resources and transcriptomic data for enrichment and network analyses to identify shared inflammatory features between MetS and HF.
Keywords:
brown adipose tissueheart failure risk phenotypemetabolic syndromeresidual inflammatory risktranscriptomics

Related Experiment Videos

  • Employed a high-fat diet (HFD) and transverse aortic constriction (TAC) mouse model to study HFpEF and brown adipose tissue (BAT) transcriptomics.

    • Main Results:

    • High RIR (hs-CRP ≥2 mg/L) was significantly associated with increased odds of an HF-risk phenotype in MetS patients.
    • Cross-disease analyses revealed shared inflammatory pathways including cytokine-chemokine activity, IL-17/TNF signaling, and ECM remodeling, with six key genes identified.
    • The mouse model exhibited an HFpEF phenotype, and BAT transcriptomics showed immune and inflammatory pathway enrichment overlapping with observed signatures.

    Conclusions:

    • In MetS, RIR is associated with a higher likelihood of an HF-risk phenotype, linked to specific inflammatory and remodeling pathways.
    • Brown adipose tissue transcriptomic data supports this inflammatory signature, suggesting a tissue-level inflammatory context.
    • Findings are associative and warrant further mechanistic studies to establish causal pathways from tissue to heart.