Mesenchymal stem cells, or MSCs, could one day help patients with myasthenia gravis (MG) regain strength and slow muscle wasting, though challenges remain before these treatments can be used widely, according to a review published recently in Frontiers in Cell and Developmental Biology.
Clinical evidence so far suggests that MSCs can protect muscle and nerve function, but their benefits in people are not yet as strong as those seen in lab studies.
“MSCs exhibit unique advantages in the treatment of MG and muscle degenerative diseases through multidimensional mechanisms,” explained this review’s authors.
MSCs have several traits that make them appealing for treating MG. These cells can renew themselves, turn into different tissue types, and regulate inflammation. In animal studies, MSCs reduced harmful immune attacks on the neuromuscular junction (the site where nerves communicate with muscles) and decreased antibodies that target acetylcholine receptors, which are key molecules needed for muscle contraction.
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Beyond calming the immune system, MSCs help repair muscle tissue. They promote the growth of satellite cells, which are muscle stem cells that regenerate damaged fibers, and release molecules that prevent further muscle loss.
MSCs also appear to stabilize communication between nerves and muscles by releasing protective factors that support motor neurons and strengthen neuromuscular connections. This dual action of reducing inflammation and aiding regeneration could make MSCs a unique therapy for restoring function in patients with MG.
However, the effectiveness of MSCs after transplantation has often fallen short of expectations. Many cells fail to survive, do not reach the damaged tissue, or lose function in an aging or inflamed environment. To overcome these obstacles, researchers are testing new strategies such as using MSCs from donor fat or umbilical cord tissue, combining them with neuroprotective drugs or embedding them in hydrogels to enhance stability and delivery.
Age-related decline in MSC function may also play a role in late-onset MG, which most often affects people in their 70s. Older, senescent MSCs are less able to regenerate muscle and more prone to causing fat buildup and fibrosis in skeletal tissue. Understanding and reversing this decline could make future cell-based therapies more effective for older patients.
If clinical studies confirm these results, MSC therapy could offer a new way to address both the immune and muscle aspects of MG, potentially improving endurance and quality of life for patients living with chronic muscle weakness.
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