Il-15

Yeghiazarians, Yerem; Honbo, Norman; Imhof, Isabella; Woods, Brandon J.; Aguilera, Vanessa; Ye, Jianqin; Boyle, Andrew; Karliner, Joel S.

doi:10.1097/fjc.0000000000000061

Cited by 22 publications

(5 citation statements)

References 28 publications

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“…6c ). The hearts of exercise-trained Atg7 h&mKO mice also had markedly reduced levels of the PPARGC1α target Fndc5 33 and the pro-survival Il15 34 (Supplementary Fig. S3c ).…”

Section: Resultsmentioning

confidence: 99%

Exercise leads to unfavourable cardiac remodelling and enhanced metabolic homeostasis in obese mice with cardiac and skeletal muscle autophagy deficiency

Yan

Kronemberger

Blomme

et al. 2017

Sci Rep

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Autophagy is stimulated by exercise in several tissues; yet the role of skeletal and cardiac muscle-specific autophagy on the benefits of exercise training remains incompletely understood. Here, we determined the metabolic impact of exercise training in obese mice with cardiac and skeletal muscle disruption of the Autophagy related 7 gene (Atg7h&mKO). Muscle autophagy deficiency did not affect glucose clearance and exercise capacity in lean adult mice. High-fat diet in sedentary mice led to endoplasmic reticulum stress and aberrant mitochondrial protein expression in autophagy-deficient skeletal and cardiac muscles. Endurance exercise training partially reversed these abnormalities in skeletal muscle, but aggravated those in the heart also causing cardiac fibrosis, foetal gene reprogramming, and impaired mitochondrial biogenesis. Interestingly, exercise-trained Atg7h&mKO mice were better protected against obesity and insulin resistance with increased circulating fibroblast growth factor 21 (FGF21), elevated Fgf21 mRNA and protein solely in the heart, and upregulation of FGF21-target genes involved in thermogenesis and fatty acid oxidation in brown fat. These results indicate that autophagy is essential for the protective effects of exercise in the heart. However, the atypical remodelling elicited by exercise in the autophagy deficient cardiac muscle enhances whole-body metabolism, at least partially, via a heart-brown fat cross-talk involving FGF21.

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“…6c ). The hearts of exercise-trained Atg7 h&mKO mice also had markedly reduced levels of the PPARGC1α target Fndc5 33 and the pro-survival Il15 34 (Supplementary Fig. S3c ).…”

Section: Resultsmentioning

confidence: 99%

Exercise leads to unfavourable cardiac remodelling and enhanced metabolic homeostasis in obese mice with cardiac and skeletal muscle autophagy deficiency

Yan

Kronemberger

Blomme

et al. 2017

Sci Rep

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“…For example, the expression level of Il15 in adult cluster A3 was found to be decreased at P7 in the Sox6 KO heart (Table 4). It has been recently demonstrated that Il15 protects cardiomyocytes from oxidative stress [114], suggesting that Il15 could be involved in protection from oxidative stress during postnatal heart development, and Sox6 could be a positive regulator of Il15 in the early postnatal heart. Lyz1 in adult cluster A4 was also differentially expressed at two time points (decreased at P7 and P30) in the Sox6 KO heart (Table 4).…”

Section: Resultsmentioning

confidence: 99%

Transcriptome Dynamics and Potential Roles of Sox6 in the Postnatal Heart

Ichihashi

Peng

et al. 2016

PLoS ONE

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The postnatal heart undergoes highly coordinated developmental processes culminating in the complex physiologic properties of the adult heart. The molecular mechanisms of postnatal heart development remain largely unexplored despite their important clinical implications. To gain an integrated view of the dynamic changes in gene expression during postnatal heart development at the organ level, time-series transcriptome analyses of the postnatal hearts of neonatal through adult mice (P1, P7, P14, P30, and P60) were performed using a newly developed bioinformatics pipeline. We identified functional gene clusters by principal component analysis with self-organizing map clustering which revealed organized, discrete gene expression patterns corresponding to biological functions associated with the neonatal, juvenile and adult stages of postnatal heart development. Using weighted gene co-expression network analysis with bootstrap inference for each of these functional gene clusters, highly robust hub genes were identified which likely play key roles in regulating expression of co-expressed, functionally linked genes. Additionally, motivated by the role of the transcription factor Sox6 in the functional maturation of skeletal muscle, the role of Sox6 in the postnatal maturation of cardiac muscle was investigated. Differentially expressed transcriptome analyses between Sox6 knockout (KO) and control hearts uncovered significant upregulation of genes involved in cell proliferation at postnatal day 7 (P7) in the Sox6 KO heart. This result was validated by detecting mitotically active cells in the P7 Sox6 KO heart. The current report provides a framework for the complex molecular processes of postnatal heart development, thus enabling systematic dissection of the developmental regression observed in the stressed and failing adult heart.

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“…IL-15 is pleiotropic proinflammatory cytokine with structural similarity with IL-2, which predominantly exerts anabolic and tissue protective effects by decreasing cardiac myocyte apoptosis, mobilization of endothelial and mesenchymal progenitor cells, reduction of oxidative stress, and improvement of myocardial function [ 149 ]. On hypoxia condition, cardiac myocytes express appropriate IL-15 receptor, by which IL-15 protects the myocardium against injury [ 149 ]. IL-15 activates signaling by the β and common γ ( γ c) chain heterodimer of the IL-2 receptor and thereby supports survival and proliferation of natural killer cells and suppresses oxidative stress [ 150 ].…”

Section: Myokines In Hf Myopathymentioning

confidence: 99%

Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes

Berezin

Lichtenauer

2021

Disease Markers

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Heart failure (HF) is a global medical problem that characterizes poor prognosis and high economic burden for the health system and family of the HF patients. Although modern treatment approaches have significantly decreased a risk of the occurrence of HF among patients having predominant coronary artery disease, hypertension, and myocarditis, the mortality of known HF continues to be unacceptably high. One of the most important symptoms of HF that negatively influences tolerance to physical exercise, well-being, social adaptation, and quality of life is deep fatigue due to HF-related myopathy. Myopathy in HF is associated with weakness of the skeletal muscles, loss of myofibers, and the development of fibrosis due to microvascular inflammation, metabolic disorders, and mitochondrial dysfunction. The pivotal role in the regulation of myocardial and skeletal muscle rejuvenation, attenuation of muscle metabolic homeostasis, and protection against ischemia injury and apoptosis belongs to myokines. Myokines are defined as a wide spectrum of active molecules that are directly synthesized and released by both cardiac and skeletal muscle myocytes and regulate energy homeostasis in autocrine/paracrine manner. In addition, myokines have a large spectrum of pleiotropic capabilities that are involved in the pathogenesis of HF including cardiac remodeling, muscle atrophy, and cardiac cachexia. The aim of the narrative review is to summarize the knowledge with respect to the role of myokines in adverse cardiac remodeling, myopathy, and clinical outcomes among HF patients. Some myokines, such as myostatin, irisin, brain-derived neurotrophic factor, interleukin-15, fibroblast growth factor-21, and growth differential factor-11, being engaged in the regulation of the pathogenesis of HF-related myopathy, can be detected in peripheral blood, and the evaluation of their circulating levels can provide new insights to the course of HF and stratify patients at higher risk of poor outcomes prior to sarcopenic stage.

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Il-15

Cited by 22 publications

References 28 publications

Exercise leads to unfavourable cardiac remodelling and enhanced metabolic homeostasis in obese mice with cardiac and skeletal muscle autophagy deficiency

Exercise leads to unfavourable cardiac remodelling and enhanced metabolic homeostasis in obese mice with cardiac and skeletal muscle autophagy deficiency

Transcriptome Dynamics and Potential Roles of Sox6 in the Postnatal Heart

Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes

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