Metrnl Dynamics in Metabolic and Cardiovascular Health

Meteorin-like hormone (Metrnl) is a secreted protein produced by skeletal muscle, adipose tissue and activated immune cells that exerts pleiotropic effects on energy homeostasis, inflammatory regulation and tissue repair. Functioning as both an adipokine and a myokine, Metrnl modulates glucose and lipid metabolism, enhances insulin sensitivity and orchestrates immunometabolic crosstalk in the cardiovascular system. In metabolic tissues, exercise- or diet-induced Metrnl release activates key signalling nodes, including AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor δ (PPARδ), to suppress inflammatory cascades, promote fatty-acid oxidation and improve glucose uptake. In the heart, Metrnl facilitates macrophage polarisation toward a reparative phenotype, attenuates ischaemia–reperfusion injury and reduces cardiomyocyte apoptosis. Clinical observational studies reveal that reduced circulating Metrnl correlates with insulin resistance, dyslipidaemia and severity of coronary artery disease, suggesting its potential as a biomarker and therapeutic target. Emerging evidence situates Metrnl at the interface of metabolic and cardiovascular health, with broad implications for the management of obesity, diabetes and ischaemic heart disease.

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Metrnl Dynamics in Metabolic and Cardiovascular Health publication trend

The graph below shows the total number of articles in metrnl dynamics in metabolic and cardiovascular health across all publications each year (not limited to Nature Index journals).

Technical terms

Metrnl (Meteorin-like): A secreted adipomyokine involved in regulating energy metabolism and immune responses.

AMPK (AMP-activated protein kinase): A cellular energy sensor that promotes catabolic pathways and suppresses inflammation when activated.

PPARδ (Peroxisome proliferator-activated receptor δ): A nuclear receptor that regulates fatty-acid oxidation and energy expenditure in muscle.

Macrophage polarisation: The functional shift of macrophages between pro-inflammatory (M1) and anti-inflammatory, tissue-repairing (M2) states.

Ischaemia–reperfusion injury: Tissue damage caused by restoration of blood flow after a period of ischaemia, commonly occurring in myocardial infarction.

WNT/β-catenin pathway: A signalling cascade that regulates cell proliferation and survival, relevant to β-cell function.

References

1. Metrnl ameliorates myocardial ischemia–reperfusion injury by activating AMPK-mediated M2 macrophage polarization. Molecular Medicine (2025).
2. Meteorin-like/Metrnl, a novel secreted protein implicated in inflammation, immunology, and metabolism: A comprehensive review of preclinical and clinical studies. Frontiers in Immunology (2023).
3. METRNL attenuates lipid-induced inflammation and insulin resistance via AMPK or PPARδ-dependent pathways in skeletal muscle of mice. Experimental & Molecular Medicine (2018).
4. Lower serum levels of Meteorin-like/Subfatin in patients with coronary artery disease and type 2 diabetes mellitus are negatively associated with insulin resistance and inflammatory cytokines. PLOS ONE (2018).
5. Serum Metrnl is associated with the presence and severity of coronary artery disease. Journal of Cellular and Molecular Medicine (2018).
6. Meteorin-Like Ameliorates β Cell Function by Inhibiting β Cell Apoptosis of and Promoting β Cell Proliferation via Activating the WNT/β-Catenin Pathway. Frontiers in Pharmacology (2021).
7. Serum Metrnl levels are decreased in subjects with overweight or obesity and are independently associated with adverse lipid profile. Frontiers in Endocrinology (2022).