Crosstalk Between Muscle and Bone Via the Muscle-Myokine Irisin

Colaianni, Graziana; Mongelli, Teresa; Colucci, Silvia; Cinti, Saverio; Grano, Maria

doi:10.1007/s11914-016-0313-4

Cited by 63 publications

(54 citation statements)

References 39 publications

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“…Colaianni, et al verified that irisin could induce the differentiation and increase activity of osteoblasts; moreover, irisin increased cortical bone mass [7][8][9]. That means irisin may be an inhibitor of vascular calcification for its capacity to promote bone formation.…”

Section: Introductionmentioning

confidence: 99%

Lower Serum Irisin Levels Are Associated with Increased Vascular Calcification in Hemodialysis Patients

Lian¹,

He²,

Lata³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Vascular calcification, which involves an active cellular transformation of vascular smooth muscle cells into bone forming cells, is prevalent and predicts mortality in dialysis patients. Its mechanisms are complex and unclear. We presume that irisin, a newly identified myokine also may play roles in vascular calcification in hemodialysis patients. This study aims to evaluate serum irisin levels and establish their relation to vascular calcification and other parameters in hemodialysis patients. Methods: A total of 150 patients on maintenance hemodialysis treatment and 38 age-and sex-matched healthy controls were enrolled in this cross-sectional study. Serum irisin concentrations were measured by ELISA. Vascular calcification was evaluated by abdominal aortic calcification scores. Results: Serum irisin concentrations were significantly lower in hemodialysis patients than in controls [52.8 (22.0, 100.0) vs. 460.8 (434.8, 483.4) ng/ml, P<0.01]. In addition, irisin was negatively correlated with the parathyroid hormone level (P=0.01). The HD patients with vascular calcification showed significantly lower serum irisin concentrations [39.0 (21.7, 86.2) vs.79.0 (39.5, 130.2) ng/mL, P<0.01]. Compared with the group without vascular calcification multivariate logistic regression analyses revealed that serum irisin, HD vintage and age were significant independent determinant factors for vascular calcification in HD patients. Conclusion: Our results are the first to provide a clinical evidence of the association between serum irisin and vascular calcification in HD patients. Lower irisin levels, long-term hemodialysis and old ages are independent risk factors in HD patients.

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Section: Introductionmentioning

confidence: 99%

Lower Serum Irisin Levels Are Associated with Increased Vascular Calcification in Hemodialysis Patients

Lian¹,

He²,

Lata³

et al. 2018

Kidney Blood Press Res

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“…With models of skeletal muscle inactivity, either because of congenital muscle disease or induced paralysis, bones and joints showed developmental alterations or increased resorption, depending on the age at muscular damage (14). Although the mechanotransduction theory has provided an explanation for understanding the effect of muscle on bone, accumulating evidence has revealed that crosstalk between muscle and bone occurs in a paracrine or endocrine fashion via myokines released by muscle (15).…”

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confidence: 99%

Irisin promotes proliferation but inhibits differentiation in osteoclast precursor cells

et al. 2018

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The receptor activator of NF-κB ligand-induced osteoclast differentiation has a critical role in the process of bone metabolism. Overactivation of osteoclastogenesis may result in a series of diseases. Irisin, a novel myokine, which was first reported in 2012, has been proposed to mediate the beneficial metabolic effects of exercise. Studies have demonstrated that irisin targets osteoblasts by promoting osteoblast proliferation and differentiation; however, the underlying mechanism regarding the effect of irisin on osteoclasts remains elusive. Using 2 types of osteoclast precursor cells, RAW264.7 cells and mouse bone marrow monocytes, we showed that irisin promoted osteoclast precursor cell proliferation but inhibited osteoclast differentiation. Irisin down-regulated the expression of osteoclast differentiation marker genes, including receptor activators of NF-κB, nuclear factor of activated T cells, cytoplasmic 1, cathepsin K, and tartrate-resistant acid phosphatase (TRAP), as well as decreasing the number of TRAP-positive multinucleated cells and hydroxyapatite resorption pits. Furthermore, we showed that irisin suppressed the NF-κB signaling pathway, but activated the p38 and JNK signaling pathways. In the presence of an inhibitor of p38 and JNK, irisin-induced promotion of RAW264.7 cell proliferation was attenuated. However, irisin-induced inhibition of osteoclast differentiation was not affected by either the p38 or JNK signaling pathway. Our study suggested the direct effect of irisin on osteoclastogenesis and revealed the mechanism responsible for the therapeutic potential of irisin in bone metabolism disease.-Ma, Y., Qiao, X., Zeng, R., Cheng, R., Zhang, J., Luo, Y., Nie, Y., Hu, Y., Yang, Z., Zhang, J., Liu, L., Xu, W., Xu, C. C., Xu, L. Irisin promotes proliferation but inhibits differentiation in osteoclast precursor cells.

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“…Irisin autocrinally modulates some metabolic functions in the skeletal muscle, and it also exerts endocrine effects on adipocytes and osteoblasts. In fact irisin can induce browning of white adipose tissue, and can regulate the expression of osteogenic genes as well as it is able to induce differentiation of osteoblasts[102]. Zhang et al[103] reported that circulating irisin was negatively associated with intrahepatic triglyceride content in Chinese obese adults with NAFLD, independent of other metabolic factors.…”

Section: Potential Mechanisms Underlying the Interplay Between Nafldmentioning

confidence: 99%

Non-alcoholic fatty liver disease connections with fat-free tissues: A focus on bone and skeletal muscle

Poggiogalle¹,

Donini²,

Lenzi³

et al. 2017

WJG

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The estimates of global incidence and prevalence of non-alcoholic fatty liver disease (NAFLD) are worrisome, due to the parallel burden of obesity and its metabolic complications. Indeed, excess adiposity and insulin resistance represent two of the major risk factors for NAFLD; interestingly, in the last years a growing body of evidence tended to support a novel mechanistic perspective, in which the liver is at the center of a complex interplay involving organs and systems, other than adipose tissue and glucose homeostasis. Bone and the skeletal muscle are fat- free tissues which appeared to be independently associated with NAFLD in several cross-sectional studies. The deterioration of bone mineral density and lean body mass, leading to osteoporosis and sarcopenia, respectively, are age-related processes. The prevalence of NAFLD also increases with age. Beyond physiological aging, the three conditions share some common underlying mechanisms, and their elucidations could be of paramount importance to design more effective treatment strategies for the management of NAFLD. In this review, we provide an overview on epidemiological data as well as on potential contributors to the connections of NAFLD with bone and skeletal muscle.

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Crosstalk Between Muscle and Bone Via the Muscle-Myokine Irisin

Cited by 63 publications

References 39 publications

Lower Serum Irisin Levels Are Associated with Increased Vascular Calcification in Hemodialysis Patients

Lower Serum Irisin Levels Are Associated with Increased Vascular Calcification in Hemodialysis Patients

Irisin promotes proliferation but inhibits differentiation in osteoclast precursor cells

Non-alcoholic fatty liver disease connections with fat-free tissues: A focus on bone and skeletal muscle

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