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The heterogeneity of MCAS, with its varied mutational profiles and aberrant expression of hundreds of potent mediators, creates chronic multisystem polymorbidity with inflammatory, allergic, and dystrophic phenotypes
Previous studies indicated that inflammation plays an important role in the development of OA, which is often closely related to low-grade synovitis [17]
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Investigations into KPV's mechanism have focused on its interaction with melanocortin 1 receptor (MC1R) and melanocortin 4 receptor (MC4R), both of which modulate inflammatory cytokine production
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