Aquaporin-4 downregulation in dysphagic patients with idiopathic inflammatory myopathies: myofiber vulnerability and inflammation drivers
Authors' conclusion
Myofiber hypotrophy appears to be due to inflammation from CD68-positive and MMP2-positive cells, whose activity disrupts the extracellular matrix and may detach AQP4 from the sarcolemma.
Study context
- Population
- Patients with IIM with and without dysphagia, and healthy controls; limb muscle biopsies
- Exposure
- IIM patients with dysphagia vs IIM patients without dysphagia vs healthy controls
- Outcome
- Percentage of AQP4-expressing myofibers
Methodological detailsmuscle biopsy immunolocalization
- Muscle biopsy immunolocalization
Main finding
As reported in the abstract
AQP4 immunostaining in myofibers
- AQP4 immunostaining significantly decreased in myofibers of dysphagic patients compared with normophagic patients and controls
Observational data: associations, not effects.
Further findings
- Both IIM groups had CD68-positive cells surrounding AQP4-negative myofibers; only in dysphagic patients were AQP4-negative myofibers surrounded by CD68-positive and MMP2-positive cells significantly increased
Original publication
Aquaporin-4 downregulation in dysphagic patients with idiopathic inflammatory myopathies: myofiber vulnerability and inflammation drivers. Rheumatology (Oxford). Published 18 August 2025. doi:10.
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