1.
Autophagy Is a Promoter for Aerobic Exercise Performance during High Altitude Training.
Zhang, Y, Chen, N
Oxidative medicine and cellular longevity. 2018;:3617508
Abstract
High altitude training is one of the effective strategies for improving aerobic exercise performance at sea level via altitude acclimatization, thereby improving oxygen transport and/or utilization. But its underlying molecular mechanisms on physiological functions and exercise performance of athletes are still vague. More recent evidence suggests that the recycling of cellular components by autophagy is an important process of the body involved in the adaptive responses to exercise. Whether high altitude training can activate autophagy or whether high altitude training can improve exercise performance through exercise-induced autophagy is still unclear. In this narrative review article, we will summarize current research advances in the improvement of exercise performance through high altitude training and its reasonable molecular mechanisms associated with autophagy, which will provide a new field to explore the molecular mechanisms of adaptive response to high altitude training.
2.
Autophagy as a target for glucocorticoid-induced osteoporosis therapy.
Shen, G, Ren, H, Shang, Q, Qiu, T, Yu, X, Zhang, Z, Huang, J, Zhao, W, Zhang, Y, Liang, D, et al
Cellular and molecular life sciences : CMLS. 2018;(15):2683-2693
Abstract
Autophagy takes part in regulating the eukaryotic cells function and the progression of numerous diseases, but its clinical utility has not been fully developed yet. Recently, mounting evidences highlight an important correlation between autophagy and bone homeostasis, mediated by osteoclasts, osteocytes, bone marrow mesenchymal stem cells, and osteoblasts, and autophagy plays a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The combinations of autophagy activators/inhibitors with anti-GIOP first-line drugs or some new autophagy-based manipulators, such as regulation of B cell lymphoma 2 family proteins and caspase-dependent clearance of autophagy-related gene proteins, are likely to be the promising approaches for GIOP clinical treatments. In view of the important role of autophagy in the pathogenesis of GIOP, here we review the potential mechanisms about the impacts of autophagy in GIOP and its association with GIOP therapy.
3.
Curcumin Suppresses Proliferation and Migration of MDA-MB-231 Breast Cancer Cells through Autophagy-Dependent Akt Degradation.
Guan, F, Ding, Y, Zhang, Y, Zhou, Y, Li, M, Wang, C
PloS one. 2016;(1):e0146553
Abstract
Previous studies have evidenced that the anticancer potential of curcumin (diferuloylmethane), a main yellow bioactive compound from plant turmeric was mediated by interfering with PI3K/Akt signaling. However, the underlying molecular mechanism is still poorly understood. This study experimentally revealed that curcumin treatment reduced Akt protein expression in a dose- and time-dependent manner in MDA-MB-231 breast cancer cells, along with an activation of autophagy and suppression of ubiquitin-proteasome system (UPS) function. The curcumin-reduced Akt expression, cell proliferation, and migration were prevented by genetic and pharmacological inhibition of autophagy but not by UPS inhibition. Additionally, inactivation of AMPK by its specific inhibitor compound C or by target shRNA-mediated silencing attenuated curcumin-activated autophagy. Thus, these results indicate that curcumin-stimulated AMPK activity induces activation of the autophagy-lysosomal protein degradation pathway leading to Akt degradation and the subsequent suppression of proliferation and migration in breast cancer cell.