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KLK15 alters connective tissues in hypermobile Ehlers-Danlos syndrome
Journal article   Open access   Peer reviewed

KLK15 alters connective tissues in hypermobile Ehlers-Danlos syndrome

Cortney Gensemer, Taylor Petrucci, Tyler Beck, Victoria Daylor, Molly Griggs, Charlotte Griggs, Amy Weintraub, Kathryn Byerly, Lilong Guo, Jordan Morningstar, …
iScience, v 28(9), 113343
19 Sep 2025
PMID: 40949095
url
https://doi.org/10.1016/j.isci.2025.113343View
Published, Version of Record (VoR) Open

Abstract

Biological process Body system Non-infectious disease Molecular Genetics
Hypermobile Ehlers-Danlos syndrome (hEDS) is a debilitating multisystem condition characterized by joint hypermobility, chronic pain, and diverse comorbidities, yet its genetic basis remains undefined. Whole-exome sequencing (WES) of 200 patients with hEDS revealed rare and low frequency variants in 14 of 15 kallikrein (KLK) genes, including a recurrent KLK15 missense variant (p.Gly226Asp) segregating in multiple families. KLK15, a secreted serine protease, is expressed in connective and immune tissues and interacts with extracellular matrix (ECM) components, including fibronectin and lysyl oxidase (LOX). A KLK15 knock-in mouse model recapitulated hEDS features in tendons and cardiac valves and exhibited dysregulated cytokine profiles. The variant altered KLK15 and LOX compartmentalization within the ECM, consistent with a dominant-negative effect. These findings identify KLK15 as a contributor to hEDS and reveal broader roles for KLK protease-ECM-immune crosstalk in connective tissue regulation. This study reframes hEDS as a condition involving matrix remodeling and immune signaling beyond collagen defects. [Display omitted] •KLK15 identified as a novel disease gene in multiple families with hEDS•Knock-in mice have tendon, skin, and heart valve abnormalities similar to patients•Knock-in mice show altered immune signaling and extracellular matrix organization•Findings expand hEDS pathogenesis to proteolytic and immune dysregulation Body system; Non-infectious disease; Biological process; Molecular genetics

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Immunology
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