Preprint Communication Version 1 Preserved in Portico This version is not peer-reviewed

Deficiency of MMP-10 Aggravates the Diseased Phenotype of Aged Dystrophic Mice

Arantxa Baraibar Churio
,
Miriam Bobadilla
ORCID logo ,
Neira Sainz
,
Florencio JD Machado
ORCID logo ,
Josune Orbe
ORCID logo ,
and Ana Pérez-Ruiz
*
Version 1 : Received: 29 October 2021 / Approved: 1 November 2021 / Online: 1 November 2021 (12:56:58 CET)

A peer-reviewed article of this Preprint also exists.

Baraibar-Churio, A.; Bobadilla, M.; Machado, F.J.D.; Sáinz, N.; Roncal, C.; Abizanda, G.; Prósper, F.; Orbe, J.; Pérez-Ruiz, A. Deficiency of MMP-10 Aggravates the Diseased Phenotype of Aged Dystrophic Mice. Life 2021, 11, 1398. Baraibar-Churio, A.; Bobadilla, M.; Machado, F.J.D.; Sáinz, N.; Roncal, C.; Abizanda, G.; Prósper, F.; Orbe, J.; Pérez-Ruiz, A. Deficiency of MMP-10 Aggravates the Diseased Phenotype of Aged Dystrophic Mice. Life 2021, 11, 1398.

Abstract

Matrix metalloproteinases have been implicated in muscular dystrophy progression and recent studies described the role of MMP-10 in skeletal muscle pathology of young dystrophic mice. Nevertheless, its implication in dystrophin deficient hearts is still missing. Here, we aimed at investigating MMP-10 implication in severe muscular dystrophic progression and characterize MMP-10 loss in skeletal and cardiac muscles of aged dystrophic mice. We examined the histopathological effect of MMP-10 ablation in aged mdx mice, both in the hind limb muscles and heart tissues. We have found that MMP-10 loss compromises survival rates of aged mdx mice, with skeletal and cardiac muscles developing a chronic inflammatory response. Our findings indicate that MMP-10 is implicated in severe muscular dystrophy progression, identifying a new area of investigation that could lead to future therapies for dystrophic muscles.

Keywords

matrix metalloproteases; muscular dystrophy; skeletal muscle; cardiac muscle

Subject

Biology and Life Sciences, Cell and Developmental Biology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Download PDF

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0
Get PDF Cite Share 0
Bookmark BibSonomy Mendeley Reddit Delicious
×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.