Metabolism Research Paper

Metabolism:
Existed evidence notified that changed in the metabolic processes including oxidative stress, mitochondrial metabolism and absorption of glucose is concerned to altered MSC differentiation. Mitochondrial metabolism and ROS generation play crucial roles in adipogenic differentiation [37, 47-49]. It has been investigated that exogenous hydrogen peroxide increased adipogenic differentiation of MSCs, while mitochondrial-targeted antioxidants decreased it. Moreover, ROS that generated through mitochondrial complex III is crucial for initiation of adipogenic transcription factors [49]. Therefore, enhanced mitochondrial metabolism is a fundamental factor and prerequisite for adipogenesis differentiation by blocking the mitochondrial respiratory pathways [47]. In addition, it has been
In addition, integrins phosphorylated the focal adhesion kinase (FAK) that activated several signaling proteins of Rho family such as protein kinase C (PKC), MAPK ERK1/2, phosphatidylinositol 3-kinase (PI3K) and GTPases [52, 53]. It has been investigated that FAK-associated activation of ERK1/2 and p38 phosphorylation activates Runx2 that enhanced the osteogenic differentiation of MC3T3-E1 cells [54]. Pref-1 inhibits adipogenic differentiation by interacting with fibronectin that followed by association with several integrin receptors to downregulates adipogenic mediated transcription factors [55, 56]. It has been investigated that mechanical forces promoted osteogenic differentiation while suppressed adipogenic differentiation of MSCs. Meanwhile, mTORC2 mechanically regulated signaling transduction or MSC differentiation. Mechanical activation of Fyn/FAK/mTORC2 signaling pathway by Fyn (a Src family kinase) reduced adipogenic differentiation of MSCs through initiating β-catenin signaling and modulate cytoskeleton through activation of Rho proteins [18, 57]. These studies concluded that perceptive of exercise therapy