Organic Osmolytes and Duchenne Muscular Dystrophy: From Homeostasis, Inflammation and Skeletal Muscle Regeneration to Therapeutic Target| Chapter 11 | Novel Research Aspects in Medicine and Medical Science Vol. 7

 In this study, we pay particular consideration to the PKA-p38MAPK-NFAT5-organic osmolytes pathway, that involves protein kinase A, mitogen-activated protein kinase, basic factor of triggered T cells 5, and organic osmolytes. Through allure control of the inflow and outflow of natural osmolytes, this route contributes significantly to the osmotic balance inevitable for optimal cell function. Duchenne burly dystrophy (DMD) is not only one of ultimate severe forms of inherited vigorous dystrophies but also the most universal hereditary neuromuscular disease. In Duchenne sturdy dystrophy (DMD), the absence of dystrophin from the dystrophin- befriended protein complex (DAPC) causes muscle membrane imbalance, which leads to myofiber necrosis, restricted regeneration, and chronic redness. The resulting disabled DAPC-joined cellular pathways have existed described both at the microscopic and the therapeutical level, with the Toll-like receptor basic factor kappa-light-chain-enhancer of activated B containers pathway (NF-KB), Janus kinase/signal transducer and activator of copy proteins, and the transforming progress factor-β pathways receiving ultimate attention. Besides, NFAT5 plays an essential role in container survival under hyperosmolar conditions, in wasted muscle conversion, and in tissue inflammation, carefully interacting with the master manager of inflammation NF-KB. We describe the difficulty of the PKA-p38MAPK- NFAT5-organic osmolytes pathway in DMD pathophysiology and determine a clear overview of that therapeutic molecules maybe of potential benefit to DMD patients. We conclude that timbre of the PKA-p38MAPK-NFAT5-organic osmolytes pathway maybe developed as supportive situation for DMD in conjunction with hereditary therapy.

Author(s) Details:

Sandrine Herbelet,
Department of Head and Skin, Ghent University and Ghent University Hospital, C. Heymanslaan 10, 9000 Ghent, Belgium.

Caroline Merckx,
Department of Neurology, Ghent University and Ghent University Hospital, C. Heymanslaan 10, 9000 Ghent, Belgium.

Boel De Paepe,
Department of Neurology, Ghent University and Ghent University Hospital, C. Heymanslaan 10, 9000 Ghent, Belgium and Neuromuscular Reference Center, Ghent University Hospital, C. Heymanslaan 10, 9000 Ghent, Belgium.

Please see the link here: https://stm.bookpi.org/NRAMMS-V7/article/view/12175