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. 2023 Jan 11;60:102606. doi: 10.1016/j.redox.2023.102606

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© 2023 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Fig. 7 — Proposed mechanisms underlying MYL4-mediated regulation of cellular autophagy function via lysosome positioning and mobility in atrial cardiomyocytes. Left panel, MYL4 promoted lysosome mobility, autophagy flux, and cell survival in the atrium. Right panel, loss of functional MYL4 caused spontaneous development of lysosome mis-distribution with atrial enlargement, increased apoptosis, and fibrotic lesions. MYL4 overexpression attenuated atrial apoptosis and fibrosis in MYL4^p.E11K rats. ER = endoplasmic reticulum; MYL4 = myosin light chain 4.