Oliver's mTOR Atlas Evidence Platform
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Madhav Nilakhanth Mugale

Toxicologist at CSIR-CDRI in Lucknow whose group studies how organs such as the liver and lung are injured and scarred, and how hormones and drugs change that process

Division of Toxicology and Experimental Medicine, CSIR-Central Drug Research Institute, Lucknow · also affiliated with the Academy of Scientific and Innovative Research (AcSIR)

Fibrosis is scarring: after repeated injury, an organ fills with stiff connective tissue and stops working well. Madhav Mugale is last author, the group leader, of a 2026 rat study on liver fibrosis caused by the toxin carbon tetrachloride (VER2026). Male rats given testosterone kept their mitochondria, the cell's power plants, in better shape, and their autophagy, the cell's recycling system, kept flowing: the protein p62 did not pile up and markers of working autophagy such as LC3B and Beclin-1 stayed higher. mTOR activity was maintained. Castrated rats did worse, with more damaged mitochondria and more cell death. The study suggests that male hormones help the liver cope with toxic injury in rats; it did not test people.

PubMed lists more than 90 papers with Mugale, all from the Division of Toxicology and Experimental Medicine at CSIR-CDRI, a national drug research institute in Lucknow, from 2019 onward. They cover safety testing of drug ingredients, models of lung and liver fibrosis, and collaborations with CDRI pharmacology groups on diabetes and insulin resistance in mice. Mugale is also affiliated with the Academy of Scientific and Innovative Research (AcSIR), which runs CSIR's doctoral programmes. No official profile page was found, so job title and training are not given.

Milestones in the Atlas

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

YearEvidenceStudy
2026 A Testosterone propionate maintains autophagic flux and mitochondrial integrity via regulation of the LC3B/p62/Beclin-1/mTOR axis in induced liver fibrosis. VER2026 Last author: led the rat study showing that testosterone preserves mitochondrial health and autophagic flux, with sustained mTOR activity, in toxin-induced liver fibrosis.

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