Endotrophin as a risk marker of mortality and kidney complications in a type 1 diabetes cohort
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Hyperglycemia triggers pathological pathways leading to fibrosis, where extracellular matrix (ECM) components are accumulated. We investigated the potential of endotrophin, a pro-fibrotic molecule generated during collagen type VI formation, as a risk marker for complications to type 1 diabetes. Endotrophin was measured in serum and urine from 1,468 persons with type 1 diabetes. Outcomes included a composite kidney endpoint, first major adverse cardiovascular event (MACE), all-cause mortality, progression of albuminuria, incident heart failure, and sight-threatening diabetic eye disease. Cox proportional hazards models adjusted for conventional risk factors were applied. A doubling of serum endotrophin was independently associated with the kidney endpoint (n = 30/1,462; hazard ratio 3.39 [95% CI: 1.98–5.82]), all-cause mortality (n = 93/1,468; 1.44 [1.03–2.0]), and progression of albuminuria (n = 80/1,359; 1.82 [1.32–2.52]), but not with first MACE, heart failure, or sight-threatening diabetic eye disease after adjustment. Urinary endotrophin was not associated with any outcome after adjustment. Serum endotrophin was a risk marker for mortality and kidney complications in type 1 diabetes. Biomarkers of ECM remodeling, such as serum endotrophin, may identify persons with active pro-fibrotic processes at risk for complications in diabetes and where antifibrotic agents may reduce this risk.
Originalsprog | Engelsk |
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Artikelnummer | 1229579 |
Tidsskrift | Frontiers in Molecular Biosciences |
Vol/bind | 10 |
ISSN | 2296-889X |
DOI | |
Status | Udgivet - 2023 |
Bibliografisk note
Funding Information:
The Innovation Fund Denmark provided research support (0172-00270B) but did not play any additional role in the study design, data collection, analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
Copyright © 2023 Møller, Tougaard, Rasmussen, Genovese, Rønn, Hansen, Karsdal and Rossing.
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