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Fig. 9 | Inflammation and Regeneration

Fig. 9

From: Immune-mediated myogenesis and acetylcholine receptor clustering promote a slow disease progression in ALS mouse models

Fig. 9

Candidate cellular mechanisms for motor unit preservation in slow-progressing ALS mice. (1) Muscle denervation induces proinflammatory MФ (M1) invasion, mediated by chemotactic signals (i.e. MCP1), in the injured tissue area to phagocytise debris and stimulate SC proliferation; (2) the conversion to anti-inflammatory MФ (M2) (activation Sirt1, AMPK, Arg1) supports the formation and growth of new myofibres; (3) myogenic regulatory factors, MyoG and MyoD, elicit AChR subunits transcription in newly formed and denervated myofibres; (4) AChR clusterisation is induced by muscle reinnervation (collateral sprouting), which occurs at both denervated and newly formed synapses; (5) the evoked response to released ACh is enhanced leading to the maintenance of motor unit function despite muscle atrophy. The lack of M1-M2 polarisation in fast-progressing ALS mice prevents myogenesis and reinnervation upon muscle denervation. Created with BioRender.com

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Inflammation and Regeneration

ISSN: 1880-8190

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