Finally, some evidence indicates that the response to variations in ROM may be muscle-specific however, this hypothesis also warrants further study. No study to date has investigated how ROM influences muscle growth of the trunk musculature. Alternatively, research on the effects of ROM for the upper limbs is limited and conflicting, precluding the ability to draw strong practical inferences. When assessing the current body of literature, it can be inferred that performing RT through a full ROM confers beneficial effects on hypertrophy of the lower body musculature vs. The methodological quality of all included studies was deemed to be “excellent” based on the modified PEDro scale. The total combined sample of the studies was n = 135, which comprised 127 men and 8 women. Six studies were identified as meeting inclusion criteria: four of these studies involved RT for the lower limbs while the other two focused on the upper extremities. Based on the available evidence, we aimed to draw evidence-based recommendations for RT prescription. partial range of motion (ROM) during dynamic, longitudinal resistance training (RT) programs on changes in muscle hypertrophy. In so doing, our results not only unravel novel aspects of neuronal biology and proteostasis but also elucidate a strategy for modulating neuronal autophagy that could be of high therapeutic potential for multiple neurodegenerative diseases.The purpose of this study was to systematically review the literature as to the effects of performing exercise with a full vs. Our findings thus establish a regulatory mechanism of autophagy intrinsic to neurons and targetable for clearing disease-related proteins in a cell-type-specific manner. Using optical pulse labeling to visualize the turnover of endogenously encoded proteins in live cells, we observed that knockdown of MTMR5 or MTMR2, but not the unrelated phosphatase MTMR9, significantly enhances neuronal degradation of TDP-43, an autophagy substrate implicated in several neurodegenerative diseases. We found that MTMR5 is necessary and sufficient to suppress autophagy in iNeurons and undifferentiated iPSCs. MTMR5 is an autophagy suppressor that acts with its binding partner, MTMR2, to dephosphorylate phosphoinositides critical for autophagy initiation and autophagosome maturation. Accordingly, we sampled nascent transcript synthesis and stabilities in fibroblasts, induced pluripotent stem cells (iPSCs), and iPSC-derived neurons (iNeurons), thereby uncovering a neuron-specific stability of transcripts encoding myotubularin-related phosphatase 5 (MTMR5). The determinants underlying poor autophagy induction in neurons and the degree to which neurons and other cell types are differentially sensitive to autophagy stimuli are incompletely defined. However, neurons respond only marginally to conventional methods for inducing autophagy, limiting efforts to develop therapeutic autophagy modulators for neurodegenerative diseases. The capacity to remove toxic proteins that accumulate in neurodegenerative disorders attests to the disease-modifying potential of the autophagy pathway. Autophagy is a conserved, multi-step process of capturing proteolytic cargo in autophagosomes for lysosome degradation.
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