ReviewInternational journal of molecular sciences2026
Pathogenesis of Shoulder Calcific Tendinopathy.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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9 authors.
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Abstract
Shoulder calcific tendinopathy is a common condition affecting adults and is has a higher incidence in women. This condition is due to a multifactorial process and is characterized by the deposition of hydroxyapatite crystals in the rotator cuff tendons. The disease shows a phenotypic transformation of tenocytes into chondrocyte-like cells, likely caused by metabolic and inflammatory changes and mechanical stress. Risk factors promoting this pathology include hyperlipidemia, advanced age, diabetes, female gender, and thyroid dysfunction. Recent studies highlight that metalloproteinases, oxidative stress, inflammatory mediators, bone morphogenetic proteins (BMPs), genetic and post-transcriptional alterations play a significant role in the pathogenesis of the disease. New therapeutic strategies are currently available that aim to modulate inflammation, osteogenic differentiation, and calcium homeostasis, showing promising results, especially in preclinical models. The aim of this review is to explore the different pathogenetic mechanisms and highlight future therapeutic developments for the treatment of shoulder calcification.
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