Oliver's mTOR Atlas Evidence Platform
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Nianyin Lv

Researcher at Nanjing University of Chinese Medicine who led a mouse study showing that the age-related loss of Lamtor5, a part of the lysosomal platform that helps switch on mTORC1, drives immune ageing through inflammation

School of Medicine, Nanjing University of Chinese Medicine (at the time of the study, 2026)

Nianyin Lv is the first author of LV2026. mTORC1, the cell's growth-control complex, is switched on at the surface of lysosomes, with the help of a protein complex called the Ragulator (LAMTOR1 to LAMTOR5) that anchors the docking machinery there. The study found that one of these proteins, Lamtor5, falls with age in macrophages, the immune cells that eat debris and germs. When Lamtor5 is lost, macrophages age early and release signals through the cGAS-STING pathway, a DNA-sensing alarm system, that spread inflammation to other tissues and push the whole body toward ageing. Putting Lamtor5 back into old mice reversed the immune ageing and eased other ageing signs. The work is in mice and gives a link between lysosomes, mTOR signalling and inflammation in old age.

PubMed shows other papers under the same initials at Nanjing University of Chinese Medicine, but they could not be tied to this researcher with confidence, so they are not used here. No official profile was found, so training and current position are not given.

Milestones in the Atlas

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

YearEvidenceStudy
2026 A Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation. LV2026 First author: showed in mice that age-related loss of the lysosomal mTOR-docking protein Lamtor5 drives macrophage ageing and body-wide ageing through cGAS-STING inflammation.

Co-authors in the Atlas 1

People with a profile here who share at least one study with Nianyin Lv.

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  • Liyun Shi Immunologist at Zhejiang Shuren University in Hangzhou whose group showed in mice that losing the lysosomal mTOR-activating protein Lamtor5 with age pushes macrophages into senescence and spreads inflammation

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