Does ROS causes benefit for skeletal muscle through mTORC1?
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Reactive oxygen species (ROS) play a dual role in skeletal muscle through mTORC1 signaling. ROS generated during physical exercise induce beneficial effects by activating mTORC1, promoting muscle adaptations like increased glucose uptake and hypertrophy . Conversely, excessive ROS levels can lead to oxidative stress, disrupting muscle integrity and function . Studies show that ATM activates TSC2 via LKB1 and AMPK in response to ROS, leading to mTORC1 suppression and induction of autophagy, a process crucial for cellular survival . Inhibition of mTORC1 by ROS-induced ATM signaling can be rescued by rapamycin, highlighting the intricate balance between ROS, mTORC1, and autophagy in skeletal muscle physiology . Therefore, ROS can indeed confer benefits to skeletal muscle through mTORC1 signaling, but the levels must be tightly regulated to prevent detrimental effects.
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| Papers (5) | Insight |
|---|---|
3 Citations | ROS triggers mTORC1 suppression, inducing autophagy in response, benefiting skeletal muscle. This pathway integrates cellular damage response with metabolic regulation, influencing cell survival. |
Open access•Dissertation 15 Dec 2015 | ROS regulate hypothalamic mTORC1, impacting food intake. Skeletal muscle benefits from ROS through mTORC1 activation are not directly addressed in the study. |
93 Citations | Mitochondrial ROS activate mTORC1, benefiting skeletal muscle by inducing autophagy during muscle differentiation, as demonstrated in the study. |
| Exercise-stimulated ROS can benefit skeletal muscle through pathways like AMPK, MAPK, NRF2, and PGC-1α, but the direct involvement of ROS in mTORC1 signaling is not addressed in the paper. | |
| Moderate levels of ROS can benefit skeletal muscle by regulating mTORC1 signaling, aiding in physiological processes. However, high ROS levels can be harmful, impacting muscle function negatively. |
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