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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">Front. Endocrinol.</journal-id>
<journal-title>Frontiers in Endocrinology</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Endocrinol.</abbrev-journal-title>
<issn pub-type="epub">1664-2392</issn>
<publisher>
<publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.3389/fendo.2023.1254977</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Endocrinology</subject>
<subj-group>
<subject>Editorial</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Editorial: Wnt signaling in endocrine and metabolic disorders</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Cailotto</surname>
<given-names>Frederic</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/537277"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-review-editing/"/>
</contrib>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Santulli</surname>
<given-names>Gaetano</given-names>
</name>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<xref ref-type="author-notes" rid="fn001">
<sup>*</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/46470"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-original-draft/"/>
</contrib>
</contrib-group>
<aff id="aff1">
<sup>1</sup>
<institution>UMR7365 Ing&#xe9;nierie Mol&#xe9;culaire et Physiopathologie Articulaire (IMOPA) Centre National de la Recherche Scientifique - Universit&#xe9; de Lorraine (CNRS-UL), Biop&#xf4;le de l&#x2019;Universit&#xe9; de Lorraine</institution>, <addr-line>Vand&#x153;uvre-l&#xe8;s-Nancy</addr-line>, <country>France</country>
</aff>
<aff id="aff2">
<sup>2</sup>
<institution>Department of Medicine, Wilf Family Cardiovascular Research Institute, Fleischer Institute for Diabetes and Metabolism (FIDAM), Albert Einstein College of Medicine</institution>, <addr-line>New York, NY</addr-line>, <country>United States</country>
</aff>
<aff id="aff3">
<sup>3</sup>
<institution>Department of Molecular Pharmacology, Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Einstein Institute for Aging Research, Institute for Neuroimmunology and Inflammation (INI), Albert Einstein College of Medicine</institution>, <addr-line>New York, NY</addr-line>, <country>United States</country>
</aff>
<author-notes>
<fn fn-type="edited-by">
<p>Edited and Reviewed by: Ralf Jockers, Universit&#xe9; Paris Cit&#xe9;, France</p>
</fn>
<fn fn-type="corresp" id="fn001">
<p>*Correspondence: Gaetano Santulli, <email xlink:href="mailto:gsantulli001@gmail.com">gsantulli001@gmail.com</email>
</p>
</fn>
</author-notes>
<pub-date pub-type="epub">
<day>07</day>
<month>08</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="collection">
<year>2023</year>
</pub-date>
<volume>14</volume>
<elocation-id>1254977</elocation-id>
<history>
<date date-type="received">
<day>08</day>
<month>07</month>
<year>2023</year>
</date>
<date date-type="accepted">
<day>24</day>
<month>07</month>
<year>2023</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#xa9; 2023 Cailotto and Santulli</copyright-statement>
<copyright-year>2023</copyright-year>
<copyright-holder>Cailotto and Santulli</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/">
<p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</p>
</license>
</permissions>
<related-article id="RA1" related-article-type="commentary-article" xlink:href="https://www.frontiersin.org/research-topics/22911" ext-link-type="uri">Editorial on the Research Topic <article-title>Wnt signaling in endocrine and metabolic disorders</article-title>
</related-article>
<kwd-group>
<kwd>Wnt</kwd>
<kwd>metabolism</kwd>
<kwd>endocrinology &amp; metabolism</kwd>
<kwd>Wnt/b-catenin</kwd>
<kwd>endocrinology</kwd>
<kwd>microRNA</kwd>
<kwd>Alzheimer&#x2019;s disease</kwd>
<kwd>cancer</kwd>
</kwd-group>
<counts>
<fig-count count="0"/>
<table-count count="0"/>
<equation-count count="0"/>
<ref-count count="10"/>
<page-count count="2"/>
<word-count count="413"/>
</counts>
<custom-meta-wrap>
<custom-meta>
<meta-name>section-in-acceptance</meta-name>
<meta-value>Cellular Endocrinology</meta-value>
</custom-meta>
</custom-meta-wrap>
</article-meta>
</front>
<body>
<p>The present Research Topic, entitled &#x201c;<italic>Wnt signaling in endocrine and metabolic disorders</italic>&#x201d; aims to emphasize the functional role of the Wnt signaling pathway in human endocrinology, focusing on metabolic disease. Endocrine and metabolic disorders encompass a wide range of conditions affecting various organ systems and physiological processes. The Wnt signaling pathway, originally recognized for its role in embryonic development and tissue homeostasis (<xref ref-type="bibr" rid="B1">1</xref>, <xref ref-type="bibr" rid="B2">2</xref>), has emerged as a crucial player in the pathogenesis of several human disorders, including cancer (<xref ref-type="bibr" rid="B3">3</xref>, <xref ref-type="bibr" rid="B4">4</xref>), and greatly contributes to disease progression and potential therapeutic implications (<xref ref-type="bibr" rid="B5">5</xref>&#x2013;<xref ref-type="bibr" rid="B7">7</xref>).</p>
<p>The first study in this Research Topic clarified that one of the mechanisms by which the &#x201c;<italic>Modified Qing&#x2019; E Formula</italic>&#x201d; (MQEF), used for more than 1,300 years in China as a treatment for lumbodynia, may exert its therapeutic effect on steroid-induced ischemic necrosis of the femoral head, is through targeting exosomal microRNAs (miRNAs) to regulate multiple signaling pathways, including Wnt, PI3K-Akt, and MAPK (<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.954778">Zhu et&#xa0;al.</ext-link>). In another original report investigating miRNAs and Wnt signaling, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.977347">Tripathi et&#xa0;al.</ext-link> demonstrate that miR-539-3p overexpression in osteoblasts downregulates several components of the Wnt signaling pathway and deteriorates trabecular microarchitecture, leading to decreased bone formation in ovariectomized mice. In the third original article in our Research Topic, a group of investigators led by Xiaolin Tu found that the small molecule C91 (CHIR99021) promotes osteogenic differentiation of bone marrow stromal cells <italic>via</italic> the activation of Wnt signaling (<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.954778">Wang et&#xa0;al.</ext-link>).</p>
<p>
<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.1021796">Vilaseca et&#xa0;al.</ext-link> provide an interesting overview of the functional roles of estrogen deficiency in the processes involved in the development of Alzheimer&#x2019;s disease, including Wnt signaling and glucose transport in the brain, amyloid precursor protein processing to form senile plaques, and Tau phosphorylation forming neurofibrillary tangles.</p>
<p>A very comprehensive review concludes our Research Topic: <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.887037">Franco et&#xa0;al.</ext-link> elegantly explain the main differences between the physiological roles of canonical Wnt signaling (essential for cell growth, tissue remodeling, and organ formation) and its pathological involvement in the development of several human diseases, including cancer. Correctly interpreting the molecular bases of Wnt signaling and metabolism, ideally in a cell-type and tissue-specific manner (<ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fendo.2022.887037">Franco et&#xa0;al.</ext-link>; <xref ref-type="bibr" rid="B8">8</xref>&#x2013;<xref ref-type="bibr" rid="B10">10</xref>), may provide formidable knowledge to biomedical scientists and clinicians, holding the promise of producing novel therapies.</p>
<p>In conclusion, understanding the intricate interplay between Wnt signaling and endocrine/metabolic disorders holds great promise for the development of targeted therapies and improved patient outcomes.</p>
<sec id="s1" sec-type="author-contributions">
<title>Author contributions</title>
<p>FC: Writing &#x2013; review &amp; editing. GS: Writing &#x2013; original draft</p>
</sec>
</body>
<back>
<sec id="s2" sec-type="funding-information">
<title>Funding</title>
<p>The Santulli Lab is supported in part by the National Institutes of Health (NIH) (the National Heart, Lung, and Blood Institute [NHLBI: R01-HL164772, R01-HL159062, R01-HL146691, and T32-HL144456 to GS] and the National Institute of Diabetes and Digestive and Kidney Diseases [NIDDK: R01-DK123259 and R01-DK033823 to GS]); the National Center for Advancing Translational Sciences (NCATS: UL1-TR002556-06 to GS); the Diabetes Action Research and Education Foundation (to GS); and the Monique Weill-Caulier and Irma T. Hirschl Trusts (to GS). FC is supported by grants from the Fondation pour la Recherche M&#xe9;dicale (FRM, n&#xb0; REP202210016152).</p>
</sec>
<sec id="s3" sec-type="COI-statement">
<title>Conflict of interest</title>
<p>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</p>
</sec>
<sec id="s4" sec-type="disclaimer">
<title>Publisher&#x2019;s note</title>
<p>All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.</p>
</sec>
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