Key result
Metabolic inflammation links cardiovascular and endocrine disorders, supporting dual-target therapies like SGLT2i and GLP-1RA.
Why the study?
Metabolic inflammation has emerged as a unifying mechanism linking cardiovascular and endocrine disorders, but a synthesis of evidence toward a unified therapeutic framework was needed.
Metabolic inflammation serves as a unifying mechanism linking cardiovascular and endocrine disorders, providing a rationale for unified therapeutic frameworks utilizing agents like SGLT2 inhibitors and GLP-1 receptor agonists.
Hypothesis-generating for dual cardio-endocrine therapies; leaves open need for RCTs before practice change.
Metabolic inflammation, or metaflammation, has emerged as a unifying mechanism linking cardiovascular and endocrine disorders. This narrative review aimed to synthesize mechanistic, clinical, and therapeutic evidence on how inflammation bridges these domains and to explore prospects for a unified therapeutic framework. We systematically searched PubMed, Scopus, and Web of Science for English-language articles published between 2010 and 2024, yielding 256 relevant articles, of which 115 were included after detailed screening. Studies addressing adipose tissue inflammation, gut microbiota dysbiosis, innate immune activation, mitochondrial dysfunction, clinical biomarkers, and anti-inflammatory therapies were analyzed. Evidence demonstrates that visceral adipose tissue (VAT) inflammation, inflammasome activation, and mitochondrial oxidative stress form shared pathogenic nodes across cardiovascular and endocrine diseases. Clinical correlates, including biomarkers such as IL-6, C-reactive protein (CRP), glycoprotein acetylation (GlycA), and exosomes, provide diagnostic and prognostic insights, while therapeutic convergence has been highlighted by sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and IL-1β-targeted interventions. Lifestyle modifications such as Mediterranean diets, microbiota-directed therapies, and intermittent fasting further reinforce dual-organ protection. Despite significant advances, limitations remain in translating multi-omics discoveries, biomarker integration, and systems pharmacology into routine practice. Current evidence underscores the need for prospective trials incorporating inflammatory phenotyping, composite cardio-endocrine outcomes, and patient-centered endpoints. Research gaps include the lack of standardized biomarkers, insufficient inclusion of diverse populations, and limited mechanistic insights from physiologically relevant models such as organ-on-chip (OoC) systems and induced pluripotent stem cell (iPSC)-derived organoids. Future studies must prioritize precision-medicine approaches and integrated care models to reduce the global burden of cardio-endocrine disease.
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Patil et al. (2026) conducted a review in Cardio-Endocrine Diseases. Metabolic inflammation acts as a unifying mechanism linking cardiovascular and endocrine disorders, supporting the use of dual-target therapies like SGLT2 inhibitors and GLP-1 receptor agonists.
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