Meteorin-like/Meteorin-β protects heart against cardiac dysfunction

Rupérez, Celia; Ferrer-Curriu, Gemma; Cervera-Barea, Aina; Florit, Laura; Guitart‐Mampel, Mariona; Garrabou, Glòria; Zamora, Mónica; Crispi, F.; Fernández‐Solà, Joaquim; Lupón, Josep; Bayés‐Genís, Antoni; Villarroya, Francesc; Planavila, Anna

doi:10.1084/jem.20201206

Cited by 44 publications

(34 citation statements)

References 48 publications

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“…A very recent study revealed that mice lacking Metrnl are prone to develop cardiac hypertrophy and Metrnl can act directly in cardiomyocytes to protect against hypertrophic processes in mice. 11 We and others previously reported that decreased serum Metrnl levels are associated with the presence and severity of coronary artery disease in humans. 12,13 However, the relationship between serum Metrnl and CHF in the elderly remains to be further elucidated.…”

Section: Introductionmentioning

confidence: 85%

“…The exact mechanism for linking Metrnl to the pathogenesis and progression of CHF is yet to be clarified. Besides muscle and adipose tissue, heart is also a source of expression and release of Metrnl 10,11 . Results from experimental studies have shown that Metrnl can attenuate doxorubicin‐induced cardiotoxicity via activating cyclic AMP/protein kinase A/Sirtuin1 pathway and reduce ischemia/reperfusion injury‐induced cardiomyocyte apoptosis via activation of AMP‐activated protein kinase/p21 activated kinase 2 signalling, 9,10 indicating that Metrnl may play important roles in cardiac repair in response to various types of injury.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that Metrnl attenuates ischaemia/reperfusion injury‐induced and doxorubicin‐induced cardiomyocyte apoptosis via activation of AMP‐activated protein kinase (AMPK)/p21 activated kinase 2 (PAK2) signalling 9 and cyclic AMP/protein kinase A pathway, 10 respectively. A very recent study revealed that mice lacking Metrnl are prone to develop cardiac hypertrophy and Metrnl can act directly in cardiomyocytes to protect against hypertrophic processes in mice 11 . We and others previously reported that decreased serum Metrnl levels are associated with the presence and severity of coronary artery disease in humans 12,13 .…”

Section: Introductionmentioning

confidence: 91%

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Serum Meteorin‐like is associated with weight loss in the elderly patients with chronic heart failure

Cai

Wang

et al. 2021

J cachexia sarcopenia muscle

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Background Unintentional weight loss (cachexia) has been associated with poor outcomes in chronic heart failure (CHF). Meteorin‐like (Metrnl) is a novel myokine with protective effects on cardiovascular diseases. However, the change of Metrnl concentrations and its role in elderly patients with CHF remains unclear. The aim of this study was to evaluate the association of serum Metrnl with weight loss and outcomes in elderly patients with CHF. Methods A total of 931 consecutive elderly patients (aged 60 years and older) with CHF and 135 age‐matched and sex‐matched control subjects were enrolled. Serum Metrnl concentration was measured by enzyme‐linked immunosorbent assay. Body weight was measured at baseline and 12 months. Results Median of serum Metrnl levels was lower in CHF patients when compared with controls [201.31 (184.95–261.16) pg/mL vs. 168.68 (103.15–197.54) pg/mL, P < 0.001]. Patients with the lowest levels of Metrnl had higher N‐terminal pro brain natriuretic peptide (NT‐proBNP) levels but lower left ventricular eject fraction (LVEF) and estimated glomerular filtration rate (P < 0.001). Lower serum Metrnl was associated with a higher risk of >5% weight loss from baseline to 12 months [odds ratio = 6.13, 95% confidence interval (CI) = 2.57–14.62 per log decrease; P < 0.001]. Serum Metrnl levels were decreased as LVEF decreased (P < 0.001) and were positively correlated with LVEF (r = 0.267, P < 0.001) but negatively correlated with NT‐proBNP levels (r = −0.257, P < 0.001). Cox regression analysis suggested that lower serum Metrnl was associated with higher cardiovascular mortality [hazard ratio (HR) = 6.71, 95% CI = 3.41–13.18 per log decrease; P < 0.001], CHF rehospitalization (HR = 3.07, 95% CI = 1.82–5.17 per log decrease; P < 0.001), and the combined major adverse cardiac event(s) (MACEs) (HR = 5.38, 95% CI = 3.51–8.25 per log decrease; P < 0.001). The Kaplan–Meier survival curves showed that low concentration of Metrnl was a prognostic indicator of MACEs in patients with CHF. Conclusions Our study suggests that lower serum Metrnl level is correlated with weight loss and the severity of cardiac dysfunction in elderly patients with CHF.

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Section: Introductionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

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Serum Meteorin‐like is associated with weight loss in the elderly patients with chronic heart failure

Cai

Wang

et al. 2021

J cachexia sarcopenia muscle

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“…It is reasonable to infer that subfatin might be a predictor of cardiac systolic dysfunction in STEMI patients. Rupérez et al [73] proposed that the specific overexpression of subfatin in the heart prevents the development of cardiac remodeling. In addition, subfatin was a novel biomarker of heart failure and had an independent prognostic value.…”

Section: Subfatin and Cadmentioning

confidence: 99%

The blooming intersection of subfatin and metabolic syndrome

Huang

Cao

Cheng

et al. 2021

Rev. Cardiovasc. Med.

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Metabolic Syndrome (MS) remains the leading cause of mortality and morbidity globally. Adipose tissue releases adipokines that play key roles in metabolic and cardio-cerebro-vascular homeostasis. Subfatin, induced after exercise or upon cold exposure in adipose tissue, is a novel secreted protein homologous to Metrn, a neutrophic factor with angiogenic properties. The protein was proved to be of great significance in the browning of white adipose tissue (BWT) and insulin resistance (IR). It affected insulin sensitivity at least via its local autocrine/paracrine action through AMP-activated protein kinase (AMPK) or peroxisome proliferator-activated receptor δ (PPAR-δ) dependent signaling. Subfatin blocked the release of inflammatory mediators, improved intracellular insulin signal transduction and reversed IR. It also improved glucose tolerance and played a key role in metabolism and cardiovascular and cerebrovascular homeostasis. It was reported that the level of serum subfatin was significantly correlated with the occurrence and severity of coronary heart disease, which might be a new target for the treatment of coronary heart disease. In addition, exercise increased the level of subfatin in circulation and adipose tissue, promoted energy consumption, improved glucose and lipid metabolism, increased the heat production of brown fat, and strengthened the anti-inflammatory mechanism. Given its role in metabolic disorders, subfatin is considered as a candidate biomarker of MS. However, the clinical significance of subfatin remains largely unclear. The purpose of this article is to review the research on the effect of subfatin on MS in recent years.

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“…METRNL is produced upon stimulation by exercise and promotes adipose tissue browning via alternative macrophage induction at adipose depots [ 22 ]. Further research revealed that METRNL plays a protective role in cardiac dysfunction and lipid-induced muscle insulin resistance by ameliorating inflammation [ 23 , 24 ]. In the present study, we used HFD-induced obese mice and isolated bone marrow-derived macrophages (BMDMs) to examine how exercise and METRNL regulate the activation of NLRP3 inflammasome.…”

Section: Introductionmentioning

confidence: 99%

Exercise Inhibits NLRP3 Inflammasome Activation in Obese Mice via the Anti-Inflammatory Effect of Meteorin-like

Javaid

Sahar

ZhuGe

et al. 2021

Cells

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Obesity is associated with chronic low-grade inflammation. The benefits of exercise are partly attributed to its anti-inflammatory effect, but whether exercise can regulate NLRP3 inflammasome activation in obese adipose tissue remains unknown. Meteorin-like (METRNL), a recently discovered myokine, has been implicated in mediating the effect of exercise on metabolism. Herein, we examined the effect of exercise and METRNL on NLRP3 inflammasome activation. High-fat diet (HFD)-induced obese mice were subjected to treadmill exercise for 8 weeks. A subgroup of HFD mice was switched to normal chow with the exercise intervention. Exercise and diet attenuated weight gain, fat accumulation, and insulin resistance in obese mice. In addition, exercise downregulated gene and protein levels of inflammasome markers, including NLRP3 and caspase-1, in adipose tissue. In isolated bone marrow-derived macrophages, activation of NLRP3 inflammasome was suppressed in the exercise group, as confirmed by the downregulation of IL-1β and IL-18. Exercise significantly enhanced the expression of METRNL in various muscle depots, and further in vitro analysis revealed that recombinant METRNL treatment inhibited IL-1β secretion in macrophages. In conclusion, exercise exerts its anti-inflammatory action by suppressing adipose tissue NLRP3 inflammasome, and this is, in part, associated with METRNL induction in muscle and its anti-inflammatory effects in macrophages.

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Meteorin-like/Meteorin-β protects heart against cardiac dysfunction

Cited by 44 publications

References 48 publications

Serum Meteorin‐like is associated with weight loss in the elderly patients with chronic heart failure

Serum Meteorin‐like is associated with weight loss in the elderly patients with chronic heart failure

The blooming intersection of subfatin and metabolic syndrome

Exercise Inhibits NLRP3 Inflammasome Activation in Obese Mice via the Anti-Inflammatory Effect of Meteorin-like

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