LKB1/AMPK deficiency aggravates mitochondrial DNA leakage via mTOR-dependent mitophagy damage in liver injury sensitized by trichloroethylene.
What this study shows
LKB1/AMPK deficiency exacerbates trichloroethylene-induced liver injury by impairing mTOR-regulated mitophagy and causing mitochondrial DNA leakage; rapamycin and AMPK activation are protective, nominating the LKB1/AMPK/mTOR axis as a candidate therapeutic target in mice; no human data.
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); 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 |
| Journal | Chemico-Biological Interactions |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-07-29 |
| Source | DOI 10.1016/j.cbi.2026.112261 · PMID 42462870 |
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 | Rapamycin; AICAR; LKB1 overexpression |
| Target | LKB1/AMPK/mTOR axis; mitophagy |
| Model | Mouse |
| Effect | Rapamycin and AMPK activation restore mTOR-dependent mitophagy; LKB1/AMPK deficiency worsens mitochondrial DNA leakage and liver injury |
In the Atlas
Related topics
Links in the pathway map
- Supports AMPK activates Mitophagy
More studies on this topic
- ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010)
- Regulation of the TSC pathway by LKB1: evidence of a molecular link between tuberous sclerosis complex and Peutz-Jeghers syndrome (2004)
- Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state (2010)
- The LKB1 tumor suppressor negatively regulates mTOR signaling (2004)
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