Impact of rAAV-shRNA treatment targeting mechanosensitive Ilk1 and Fermt2 in a mouse model of sepsis-induced muscle weakness.

ABSTRACT:

Introduction

Intensive-care-unit-acquired-muscle-weakness is a debilitating complication of sepsis, characterized by loss of muscle mass and functionality. Immobilization is an important trigger, but the role of disturbed mechanical signaling is incompletely understood. In health, the integrin-receptor-complex with key components Kindlin2 (KIND2/Fermt2) and integrin-linked-kinase (ILK/Ilk1) converses mechanical forces into biochemical signals to regulate muscle mass. We hypothesize that this complex, through key elements KIND2 and ILK, plays a role in sepsis-induced-muscle-weakness.

Methods

AAV2/9-vectors expressing shRNA-sequences against Ilk1, Fermt2 or noncoding-control-gene were injected in tibialis anterior (TA) muscles of 24w-old male C57BL/6J mice. Two-weeks-post-inje

SUBMITTER: Pacolet A 

PROVIDER: S-EPMC12700450 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature