Abstract
Irisin, a PGC1α-dependent myokine, was once believed to have beneficial effects induced by exercise. Since its first discovery of adipose browning in 2012, multiple studies have been trying to explore the metabolic functions of irisin, such as glucose and lipid metabolism. However, recently many studies with irisin concentration measuring were doubt for methodological problems, which may account for the continuous inconsistencies. New tools like recombinant irisin and gene-knockout mice are required to reconfirm the questioned functions of irisin. In this paper, we make a critical introduction to the latest researches concerning the relationship between irisin and coronary heart disease, which includes atherosclerosis, stable angina pectoris and acute coronary syndromes. These studies provided various controversial evidence of short and long-term monitoring and therapeutic effect from molecular cellular mechanisms, in vivo experiments and epidemiological investigation. But with ambiguities, irisin still has a long way to go to identify its functions in the clinical management.
Highlights
IrisinIrisin is a relatively newly discovered myokine, a small protein with 112 amino acids
Raschke et al found that start codon of fibronectin type III domain-containing protein 5 (FNDC5) gene is different, and doubted whether it’s appropriate to translate all the beneficial effect observed in mice to humans [3]
In a study based on a Japanese male population [64], the authors found that if cardiometabolic risk factors are taken into account, irisin had nothing to do with the prevalence of coronary artery calcification, but was related to progression
Summary
Irisin is a relatively newly discovered myokine, a small protein with 112 amino acids. Browning of white adipose tissue (WAT), a major effect of irisin, was observed only in inguinal WAT of training mice and attenuated in FNDC5 knockout mice [12, 13], while cold exposure was effective for all adipose depots in murine [14] When it comes to human, current evidence are not qualified enough to confirm the irisin’s responses to exercise [15,16,17,18,19,20]. In brown adipose tissue, the uncoupling protein 1 (UCP1) could release the storage of energy generated by oxidation in the form of heat and reduce the production of ATP simultaneously [26] These metabolic effects could be achieved by activating p38 MAPK and ERK pathways [27]. Irisin has participated in the development of CHD in a variety of ways, which is likely to lay a theoretical foundation for the clinical application of irisin as a biomarker or treatment
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