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Comment
. 2021 Jan:93:102328.
doi: 10.1016/j.ceca.2020.102328. Epub 2020 Dec 8.

A cellular protection racket: How lysosomal Ca2+ fluxes prevent kidney injury

Antony Galione  1 , Lianne C Davis  2 , Anthony J Morgan  2
Affiliations
Comment

A cellular protection racket: How lysosomal Ca2+ fluxes prevent kidney injury

Antony Galione et al. Cell Calcium. 2021 Jan.

Abstract

LC3-lipidation is activated by lysosomal damage by mechanisms that are unknown and divergent from canonical autophagy. In this study, Nakamura et al, show that lysosomal damage induced by lysosomotropic agents or oxalate in renal proximal tubule cells causes lipidated LC3 to insert into the lysosomal membrane to activate TRPML1 channels and release Ca2+ from lysosomes. This leads to TFEB dephosphorylation and translocation into the nucleus which results in clearance of damaged lysosomes and their contents which may reduce the deleterious effects of crystal nephropathy.

Keywords: Calcium; Crystal nephropathy; LC3; TFEB; TRPML1; mTORC1.

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  • LC3 lipidation is essential for TFEB activation during the lysosomal damage response to kidney injury.
    Nakamura S, Shigeyama S, Minami S, Shima T, Akayama S, Matsuda T, Esposito A, Napolitano G, Kuma A, Namba-Hamano T, Nakamura J, Yamamoto K, Sasai M, Tokumura A, Miyamoto M, Oe Y, Fujita T, Terawaki S, Takahashi A, Hamasaki M, Yamamoto M, Okada Y, Komatsu M, Nagai T, Takabatake Y, Xu H, Isaka Y, Ballabio A, Yoshimori T. Nakamura S, et al. Nat Cell Biol. 2020 Oct;22(10):1252-1263. doi: 10.1038/s41556-020-00583-9. Epub 2020 Sep 28. Nat Cell Biol. 2020. PMID: 32989250

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