Rapamycin-induced fatty liver in mice is attenuated by chloroquine co-treatment in an ERRα-dependent manner
What this study shows
Chloroquine co-treatment attenuates rapamycin-induced hepatic steatosis (a known mTORC1-inhibitor side effect) in mice, and this rescue depends on the nuclear receptor ERRα; RNA-seq shows chloroquine reverses rapamycin-driven upregulation of lipid-metabolism genes, with ERRα identified as a top transcriptional regulator of the effect.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (rapamycin-induced MASLD model; ERRα-null mice)); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse (rapamycin-induced MASLD model; ERRα-null mice) |
| Journal | Journal of Endocrinology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1530/JOE-26-0176 · PMID 42544714 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Chloroquine co-treatment with rapamycin |
| Target | ERRα (Esrra) / mTORC1 |
| Model | Mouse |
| Effect | Chloroquine co-treatment attenuates rapamycin-induced hepatic steatosis in an ERRα-dependent manner |
In the Atlas
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