ReviewNature metabolism2026
Metabolic Messengers: endotrophin.
Review in Nature metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotrophin (ETP), a C-terminal cleavage fragment of the collagen VI α3 chain, has emerged as a key mediator of fibroinflammation and a clinically relevant biomarker of disease progression. Accumulating evidence from both preclinical models and human studies implicates elevated ETP levels as a driver of tissue remodelling, metabolic dysfunction, inflammation and fibrosis across multiple organ systems. Increased ETP has been linked to obesity-associated adipose tissue dysfunction, steatotic liver disease, breast cancer progression, chronic kidney disease and cardiovascular disease, underscoring its broad pathological relevance. The convergence of mechanistic and clinical data positions ETP as a promising therapeutic target across a range of diseases linked by common ETP-driven dysfunction. Here we synthesize current knowledge of ETP's regulation and functions, critically evaluate its role in diverse disease contexts and outline key unanswered questions and emerging strategies for therapeutic intervention.
Identifiers
43003920What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.