ArticleExperimental & molecular medicine2025
ETP-specific-knockout mice reveal endotrophin as a key regulator of kidney fibrosis in ischemia-reperfusion injury models.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed.
- Myeloid MMP14 couples extracellular proteolysis to inflammatory and metabolic remodeling during obesity.Cell reports · 2026Article
- Diarylpropionitrile, a selective agonist of estrogen receptor β, protects the kidney against ischemia-reperfusion injury and enhances the repair of tubular epithelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Role ofCancers · 2025Review
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Abstract
Endotrophin (ETP), a cleavage product of the C5 domain of collagen VI α3 (COL6A3), plays a crucial role in extracellular matrix remodeling. Previously established Col6a3-knockout mouse models primarily reflect the consequences of COL6A3 loss rather than the specific effects of ETP depletion, making it challenging to directly assess the functions of ETP. These models either disrupt COL6A3 along with ETP production or express functionally defective COL6A3 while maintaining ETP production. Here we developed and validated a novel ETP-knockout (ETP
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