Author

Liyang Ni

The University of Tokyo

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Pharmacology & Toxicology· 2 Biochemistry· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Organism:human· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

Makoto ShimizuiD· 3 shared Ryuichiro SatoiD· 3 shared Yoshio YamauchiiD· 3 shared Hidetoshi SakuraiiD· 2 shared Lirong Zheng· 2 shared Xiaolin ZhaoiD· 2 shared Yu TakahashiiD· 2 shared Mariko Matsuto· 1 shared

Activity by Year

2025-2025 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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3 shared papersPharmacology & Toxicology

Makoto ShimizuORCID

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3 papers

Recent·Most cited

Selective induction by statins of FAM134B-mediated sarcoplasmic reticulum (SR)-phagy degrades the SR calcium pump SERCA1 and contributes to myopathy

Liyang Ni, Xiaolin Zhao, Lirong Zheng, Makoto Shimizu, Takashi Sasaki, Hidetoshi Sakurai, Ryuichiro Sato, Yoshio Yamauchi

This study identifies FAM134B-mediated SR-phagy as a mechanism by which statins induce myopathy by degrading SERCA1.

bioRxiv · Nov 26, 2025 · PreprintPharmacology & Toxicology

Modeling statin-induced myopathy with human iPSCs reveals that impaired proteostasis underlies the myotoxicity and is targetable for the prevention

Xiaolin Zhao, Liyang Ni, Miharu Kubo, Mariko Matsuto, Hidetoshi Sakurai, Makoto Shimizu, Yu Takahashi, Ryuichiro Sato, Yoshio Yamauchi

This study uses human iPSC-derived myocytes to model statin-induced myopathy, showing statins impair proteostasis via the mevalonate pathway and identify FOXO1 as a target for prevention.

American Journal of Physiology-Cell Physiology · Mar 8, 2025Peer-reviewedPharmacology & Toxicology

Fibroblast growth factor 21 regulates neuromuscular junctioninnervation through HDAC4 in denervation-induced skeletal muscle atrophy

Lirong Zheng, Takashi Sasaki, Liyang Ni, Yu Takahashi, Yoshio Yamauchi, Makoto Shimizu, Ryuichiro Sato

This study identifies FGF21 as a key driver of denervation-induced skeletal muscle atrophy through HDAC4 regulation, showing that inhibiting FGF21 could mitigate muscle atrophy.

bioRxiv · Feb 18, 2025 · PreprintBiochemistry