Study record
The DNA-dependent protein kinase catalytic subunit exacerbates endotoxemia-induced myocardial microvascular injury by disrupting the MOTS-c/JNK pathway and inducing profilin-mediated lamellipodia degradation
Zou R, Shi W, Chang X et al. · Theranostics · 2024
What this study reported
Reported that lipopolysaccharide increased DNA-PKcs activity in mouse cardiac microvascular endothelial cells and repressed MOTS-c transcription, while endothelial DNA-PKcs deletion or inhibition reduced microvascular dysfunction. In the same models, MOTS-c supplementation was associated with better endothelial barrier function, and loss of MOTS-c allowed JNK to phosphorylate profilin and destabilise lamellipodia.
Limitations
Single acute endotoxemia model with group sizes, sex and blinding not reported; the mechanism is inferred from proteomics plus pharmacological inhibitors and a mutant construct in one cell type.
Study record
| Study model | Animal study (in vivo) |
|---|---|
| Substance studied | SeveralMore than one of these is central to the paper (common for reviews). |
| Species | mouse |
| System studied | Endothelial cell-specific DNA-PKcs knockout mice given lipopolysaccharide, and cardiac microvascular endothelial cells |
| Population | Not reported |
| Design | Controlled animal experiment with cell and proteomic assays |
| Sample size as reported | Not reported |
| Control group | wild-type lipopolysaccharide-treated mice and untreated cells |
| Route (data field only) | Not reported |
| Endpoints measured | myocardial microvascular function; endothelial barrier function; MOTS-c transcription; JNK activity and profilin phosphorylation; mitochondrial fission |
| Pathways measured | MAPK signalling · Inflammation |
| Research areas | Cardiovascular · Inflammation & immunity |
| Evidence tier | C — Animal in vivo |
| Publication types | Journal Article, Research Support, Non-U.S. Gov't |
Appraisal
Each dimension is recorded separately and never combined into a single score. A study can be well controlled and still tell you little about people.
- Relevance to MOTS-c
- Direct
- Model applicability
- Mammalian
- Sample size
- Not reported
- Controls
- Appropriate
- Outcome validity
- Surrogate
- Support for its own conclusion
- Moderate
Provenance
- Bibliographic fields retrieved from PubMed E-utilities efetch (title, journal, date, authors, DOI) on 2026-11-11.
- Annotated from the published abstract.
- Editorial review: approved (2026-11-11).
- Classification follows the site methodology; the record describes the study, not what MOTS-c does in people.