Tuere Wilder

Tenofovir Causes Bone Loss via Decreased Bone Formation and Increased Bone Resorption, Which Can Be Counteracted by Dipyridamole in Mice

Endogenous adenosine maintains cartilage homeostasis and exogenous adenosine inhibits osteoarthritis progression

The antiviral drug tenofovir, an inhibitor of Pannexin-1-mediated ATP release, prevents liver and skin fibrosis by downregulating adenosine levels in the liver and skin

Adenosine A2a Receptor Blockade Diminishes Wnt/β-Catenin Signaling in a Murine Model of Bleomycin-Induced Dermal Fibrosis

Ticagrelor regulates osteoblast and osteoclast function and promotes bone formation in vivo <i>via</i> an adenosine‐dependent mechanism

Adenosine A2B receptors play an important role in bone homeostasis

Netrin‐1 and its receptor Unc5b are novel targets for the treatment of inflammatory arthritis

Bone regeneration in critical bone defects using three‐dimensionally printed β‐tricalcium phosphate/hydroxyapatite scaffolds is enhanced by coating scaffolds with either dipyridamole or BMP‐2

Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors

Netrin-1 is highly expressed and required in inflammatory infiltrates in wear particle-induced osteolysis

Brief Report: Methotrexate Prevents Wear Particle–Induced Inflammatory Osteolysis in Mice Via Activation of Adenosine A_2A Receptor

Adenosine is required for sustained inflammasome activation via the A2A receptor and the HIF-1α pathway

Adenosine regulates bone metabolism <i>via</i> A ₁ , A _2A , and A _2B receptors in bone marrow cells from normal humans and patients with multiple myeloma

Extracellular Generation of Adenosine by the Ectonucleotidases CD39 and CD73 Promotes Dermal Fibrosis

Adenosine A_2AReceptor Activation Prevents Wear Particle–Induced Osteolysis