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Reply to “Wnt/beta-catenin signaling inhibitors and nonalcoholic fatty liver disease: Potential therapeutic implications” |
Karthik Shree Harini, Devaraj Ezhilarasan ∗ |
Department of Pharmacology, Molecular Medicine and Toxicology Lab, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences
(SIMATS), Chennai, Tamil Nadu 600 077, India
∗ Corresponding author.
E-mail address: ezhild@gmail.com (D. Ezhilarasan). |
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Abstract We sincerely appreciated the interest of Polyzos et al., in our review article and sharing their improvised thoughts regarding the Wnt signaling modulators for the treatment of postmenopausal women with osteoporosis and nonalcoholic fatty liver disease (NAFLD). Several experimental studies have showed that the aberrant Wnt/ β-catenin signaling promotes the development and/or progression of a variety of chronic liver diseases including NAFLD [1,2]. Therefore, our review emphasized on the modulation of Wnt/ β-catenin signaling and the role of its mediators in NAFLD progression. Given that NAFLD prevalence is constantly increasing, and that osteoporosis is associated with women over 50 years of age with NAFLD [3] , there is an unmet need for an effective treatment. Sclerostin blocks the canonical Wnt signaling pathway of bone formation. Therefore, romosozumab, a humanized antisclerostin monoclonal antibody, was approved for the treatment of osteoporosis. Romosozumab binds to sclerostin, permitting the engagement of Wnt ligands with their co-receptors, resulting in an increase in bone formation and bone mineral density.
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