Asymptomatic Hyperuricemia Is Associated with Achilles Tendon Rupture through Disrupting the Normal Functions of...

Area of Science:

• Biochemistry
• Orthopedics
• Cell Biology

Background:

• Hyperuricemia is a metabolic disorder linked to gout.
• Increasing prevalence of hyperuricemia and observed tendon damage in asymptomatic individuals.
• The impact of hyperuricemia on tendon homeostasis remains unclear.

Purpose of the Study:

• Investigate the association between asymptomatic hyperuricemia and Achilles tendon rupture (ATR).
• Determine the pathological effects of hyperuricemia on tendon stem/progenitor cells (TSPCs).

Main Methods:

• Compared serum uric acid (SUA) levels in Achilles tendon rupture patients and healthy volunteers.
• Conducted in vitro studies on rat Achilles TSPCs exposed to uric acid (UA).
• Utilized a rat model of hyperuricemia and performed transcriptome analysis.

Main Results:

• Elevated SUA levels in ATR patients compared to controls.
• UA reduced TSPC viability, collagen expression, and structural integrity, while increasing matrix degradation and inflammation.
• Hyperuricemia model showed disrupted tendon integrity, immune cell infiltration, and altered AKT-mTOR/autophagy pathways in TSPCs.

Conclusions:

• Asymptomatic hyperuricemia may predispose individuals to Achilles tendon rupture.
• Hyperuricemia impedes normal TSPC functions, contributing to tendon pathology.
• Findings provide a basis for early prevention and care strategies for ATR.