[Matrix metalloproteinases-1, -13 and their tissue inhibitor-1 in endocrine ophthalmopathy]

E S Taskina1, S V Kharintseva1

  • 1Chita State Medical Academy.

Problemy Endokrinologii
|May 16, 2019
PubMed

Insights

Graves' ophthalmopathy (GO) involves an imbalance in matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinases-1 (TIMP-1), contributing to fibrosis. Treatment can normalize these markers, though levels may remain elevated compared to controls.

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Biochemistry

Background:

  • Graves' ophthalmopathy (GO) involves soft orbital tissue damage and fibrosis, driven by extracellular matrix remodeling.
  • Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) regulate extracellular matrix homeostasis.
  • The specific biochemical mechanisms of fibrogenesis in GO's extraocular muscles and retrobulbar tissues are not fully understood.

Purpose of the Study:

  • To investigate the biochemical mechanisms underlying extraocular muscle and retrobulbar tissue fibrogenesis in patients with Graves' ophthalmopathy.
  • To assess the levels of MMP-1, MMP-13, TIMP-1, sulfated glycosaminoglycans (sGAG), and TSHRAbs in different phases of GO.

Main Methods:

  • A study involving 65 participants (32 GO patients, 18 autoimmune thyroid patients without GO, 15 healthy controls).
  • Comprehensive ophthalmologic examinations and blood sampling for biochemical marker analysis.
  • Statistical analysis using Statistica 10.0 software.

Main Results:

  • Elevated MMP-13 levels were observed in all GO patients, with a significant increase in active GO compared to controls.
  • Pulse glucocorticoid therapy reduced MMP-13, TIMP-1, and TSHRAbs in active GO patients.
  • In inactive GO, MMP-13 remained elevated while TIMP-1 returned to reference values; MMP-1 levels did not differ significantly across groups.

Conclusions:

  • An imbalance between MMP-13 and TIMP-1 production characterizes different activity phases of Graves' ophthalmopathy.
  • Active GO shows increased serum MMP-13 and TIMP-1, suggesting dysregulated matrix remodeling contributes to fibrosis.
  • Therapeutic interventions can modulate these markers, but further research is needed to fully understand their role in GO pathogenesis.

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