Preprint Communication Version 1 Preserved in Portico This version is not peer-reviewed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

DOI: 10.3390/life11121398

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

LIFE SCIENCES, Cell & 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.

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