PUBLICATION

Dynamics of collagen oxidation and cross linking in regenerating and irreversibly infarcted myocardium

Authors
Akam-Baxter, E.A., Bergemann, D., Ridley, S.J., To, S., Andrea, B., Moon, B., Ma, H., Zhou, Y., Aguirre, A., Caravan, P., Gonzalez-Rosa, J.M., Sosnovik, D.E.
ID
ZDB-PUB-240611-4
Date
2024
Source
Nature communications   15: 46484648 (Journal)
Registered Authors
Gonzalez-Rosa, Juan Manuel
Keywords
none
MeSH Terms
  • Cicatrix/metabolism
  • Cicatrix/pathology
  • Mice
  • Disease Models, Animal
  • Collagen*/metabolism
  • Mice, Inbred C57BL
  • Male
  • Animals
  • Regeneration*
  • Myocardial Infarction*/metabolism
  • Myocardial Infarction*/pathology
  • Fluorescent Dyes/chemistry
  • Zebrafish*
  • Myocardium*/metabolism
  • Myocardium*/pathology
  • Oxidation-Reduction*
PubMed
38858347 Full text @ Nat. Commun.
Abstract
In mammalian hearts myocardial infarction produces a permanent collagen-rich scar. Conversely, in zebrafish a collagen-rich scar forms but is completely resorbed as the myocardium regenerates. The formation of cross-links in collagen hinders its degradation but cross-linking has not been well characterized in zebrafish hearts. Here, a library of fluorescent probes to quantify collagen oxidation, the first step in collagen cross-link (CCL) formation, was developed. Myocardial injury in mice or zebrafish resulted in similar dynamics of collagen oxidation in the myocardium in the first month after injury. However, during this time, mature CCLs such as pyridinoline and deoxypyridinoline developed in the murine infarcts but not in the zebrafish hearts. High levels of newly oxidized collagen were still seen in murine scars with mature CCLs. These data suggest that fibrogenesis remains dynamic, even in mature scars, and that the absence of mature CCLs in zebrafish hearts may facilitate their ability to regenerate.
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