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Muscular Dystrophy - U.S. Department of Veterans Affairs

Summarized by Plex Scholar
Last Updated: 09 March 2022

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Myeloid mineralocorticoid receptors contribute to skeletal muscle repair in muscular dystrophy and acute muscle injury.

In Duchenne muscular dystrophy mouse models, suppressing mineralocorticoid receptor response with MR antagonists is therapeutic for chronic skeletal muscle pathology. Although the mechanisms that underpin clinical MR antagonist efficacy for DMD cardiomyopathy and other cardiac disorders are well understood, muscle mechanics in skeletal muscles are yet to be fully understood. Myofiber MR knockout increases skeletal muscle strength and a subset of dystrophic pathology, which contributes to an increased sense of dystrophic pathology. We did parallel analyses of muscle function and disease to determine the role of myeloid MR in muscular muscle function and disease in skeletal muscle tissue function and disease, cytokine levels, and myeloid cell populations resulting from myeloid MR genetic loss in muscular dystrophy and acute muscle injury. In acute muscle injury, myeloid MR knockout led to increased local muscle levels of the enzyme that makes the endogenous MR agonist aldosterone, which is further supporting the importance of MR signaling in normal muscle repair. Myeloid MR knockout raised cytokine levels in muscular dystrophy, myeloid MR knockout have differed between quadriceps and diaphragm muscles, which have differing myeloid populations.

Source link: https://doi.org/10.1152/ajpcell.00411.2021

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions