Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2022, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2022/1740770
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Funding
- Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China [LHDMZ22H050001]
- Construction of Key Projects by Zhejiang Provincial Ministry [WKJ-ZJ-2017]
- Zhejiang Province Chinese Medicine Modernization Program [2020ZX001]
- Key Project of Scientific Research Foundation of Chinese Medicine [2022ZZ002]
- Pioneer and Leading Goose R&D Program of Zhejiang [2022C03118]
- Key Project of Basic Scientific Research Operating Funds of Hangzhou Medical College [KYZD202002]
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This study reveals that MC-derived exosomal miR-4455 is a key factor in regulating podocyte injury and provides potential therapeutic targets for treating IgA nephropathy.
Growing evidence suggests that mesangial cells (MCs) play a crucial role in the pathogenesis of IgA nephropathy (IgAN) by secreting aIgA1. However, the mechanism by which MCs regulate podocyte injury remains unknown. This study demonstrated that MC-derived exosomes treated with aIgA1 induced podocyte injury in IgA nephropathy. miR-4455, which was significantly upregulated in aIgA1 treatment MC-derived exosomes, can be transferred from MCs to podocytes via exosomes. MC-derived exosomal miR-4455 induced podocyte injury. Mechanistically, exosomal miR-4455 directly targeted ULK2 to regulate LC3II/I and P62 levels, which mediates autophagy homeostasis. This study revealed that MC-derived exosomal miR-4455 is a key factor affecting podocyte injury and provides a series of potential therapeutic targets for treating IgA nephropathy.
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