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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">Front. Urol.</journal-id>
<journal-title>Frontiers in Urology</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Front. Urol.</abbrev-journal-title>
<issn pub-type="epub">2673-9828</issn>
<publisher>
<publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.3389/fruro.2023.1272592</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Urology</subject>
<subj-group>
<subject>Editorial</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Editorial: Benign prostatic hyperplasia and overactive bladder: new members of metabolic syndrome</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Wang</surname>
<given-names>Xiaolong</given-names>
</name>
<xref ref-type="aff" rid="aff1">
<sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2">
<sup>2</sup>
</xref>
<xref ref-type="author-notes" rid="fn001">
<sup>*</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/1513354"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-original-draft/"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Yu</surname>
<given-names>Qingfeng</given-names>
</name>
<xref ref-type="aff" rid="aff3">
<sup>3</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/1856291"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-review-editing/"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Michel</surname>
<given-names>Martin C.</given-names>
</name>
<xref ref-type="aff" rid="aff4">
<sup>4</sup>
</xref>
<uri xlink:href="https://loop.frontiersin.org/people/9598"/>
<role content-type="https://credit.niso.org/contributor-roles/writing-review-editing/"/>
</contrib>
</contrib-group>
<aff id="aff1">
<sup>1</sup>
<institution>Department of Urology, Zhongnan Hospital of Wuhan University</institution>, <addr-line>Wuhan</addr-line>, <country>China</country>
</aff>
<aff id="aff2">
<sup>2</sup>
<institution>Department of Pathology and Laboratory Medicine, Temple University</institution>, <addr-line>Philadelphia, PA</addr-line>, <country>United States</country>
</aff>
<aff id="aff3">
<sup>3</sup>
<institution>Department of Urology, The First Affiliated Hospital of Guangzhou Medical University</institution>, <addr-line>Guangzhou</addr-line>, <country>China</country>
</aff>
<aff id="aff4">
<sup>4</sup>
<institution>Department of Pharmacology, Johannes Gutenberg University</institution>, <addr-line>Mainz</addr-line>, <country>Germany</country>
</aff>
<author-notes>
<fn fn-type="edited-by">
<p>Edited by: Giorgio Ivan Russo, University of Catania, Italy</p>
</fn>
<fn fn-type="edited-by">
<p>Reviewed by: Carmen Emanuela Scandura, Ospedale San Bassiano, Italy</p>
</fn>
<fn fn-type="corresp" id="fn001">
<p>*Correspondence: Xiaolong Wang, <email xlink:href="mailto:nogardinmunich@gmail.com">nogardinmunich@gmail.com</email>
</p>
</fn>
</author-notes>
<pub-date pub-type="epub">
<day>25</day>
<month>08</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="collection">
<year>2023</year>
</pub-date>
<volume>3</volume>
<elocation-id>1272592</elocation-id>
<history>
<date date-type="received">
<day>04</day>
<month>08</month>
<year>2023</year>
</date>
<date date-type="accepted">
<day>17</day>
<month>08</month>
<year>2023</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright &#xa9; 2023 Wang, Yu and Michel</copyright-statement>
<copyright-year>2023</copyright-year>
<copyright-holder>Wang, Yu and Michel</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/41170" ext-link-type="uri">Editorial on the Research Topic<article-title>Benign prostatic hyperplasia and overactive bladder: new members of metabolic syndrome</article-title>
</related-article>
<kwd-group>
<kwd>metabolic syndrome</kwd>
<kwd>prostate</kwd>
<kwd>hyperplasia</kwd>
<kwd>overactive bladder</kwd>
<kwd>lower urinary tract symptoms</kwd>
</kwd-group>
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<fig-count count="0"/>
<table-count count="0"/>
<equation-count count="0"/>
<ref-count count="0"/>
<page-count count="3"/>
<word-count count="953"/>
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<custom-meta-wrap>
<custom-meta>
<meta-name>section-in-acceptance</meta-name>
<meta-value>Male Urology</meta-value>
</custom-meta>
</custom-meta-wrap>
</article-meta>
</front>
<body>
<p>Benign prostatic hyperplasia (BPH) and overactive bladder syndrome (OAB) represent highly prevalent conditions, particularly in the elderly that frequently culminate in bothersome lower urinary tract symptoms (LUTS) and reduced quality of life. The intricate pathophysiology underlying these disorders remains incompletely defined, with myriad contributory factors at play. Nevertheless, an accumulating body of evidence underscores previously unrecognized roles for metabolic aberrations linked to metabolic syndrome (MetS) and associated disorders such as diabetes or arterial hypertension as relevant factors linked to LUTS in BPH and OAB. This editorial synthesizes emerging clinical and preclinical data that unveil novel mechanistic connections between metabolic dysregulation and lower urinary tract dysfunction.</p>
<sec id="s1">
<title>Clinical correlations between MetS and LUTS severity</title>
<p>Within this aggregate of investigations, quantitative correlations have been established between individual components of MetS and exacerbated LUTS. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fphar.2023.1144470">M&#xfc;derrisoglu et&#xa0;al.</ext-link> demonstrated associations of diabetes and hypertension with more pronounced baseline LUTS and attenuated therapeutic responses in OAB patients. Furthermore, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fphar.2023.1118730">Erdogan et&#xa0;al.</ext-link> discovered increased bladder weight, across five murine models exhibiting comorbid obesity and/or diabetes. These preclinical findings corroborate the putative role of metabolic abnormalities in aggravating LUTS.</p>
</sec>
<sec id="s2">
<title>Broader systemic impacts on the cardiovascular system</title>
<p>Explorations of clinical data by <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fruro.2023.1113054">Chan et&#xa0;al.</ext-link> revealed correlations between LUTS, especially nocturia, arterial stiffness, and major adverse cardiovascular events in males with MetS. This relationship implies broader systemic impacts of MetS on both the urinary and cardiovascular systems, potentially mediated by shared pathophysiological mechanisms. However, <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fphar.2022.1081074">Michel et&#xa0;al.</ext-link> identified only a weak association between hypertension and baseline LUTS/treatment outcomes (similar to the work of <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3389/fphar.2023.1144470">M&#xfc;derrisoglu et&#xa0;al.</ext-link>), underscoring the complexity of interactions between cardiovascular and metabolic components and LUTS pathogenesis.</p>
</sec>
<sec id="s3">
<title>Dissecting the multifaceted mechanistic underpinnings</title>
<p>The cumulative evidence robustly indicates MetS likely promotes the development of LUTS linked to BPH and OAB via intricate, multifactorial pathways culminating in atherosclerosis and reduced tissue perfusion. Specific MetS characteristics, particularly obesity, diabetes, and arterial stiffness, appear strongly correlated with LUTS severity, emphasizing the need to define discrete molecular mechanisms to enable targeted therapeutic development.</p>
</sec>
<sec id="s4">
<title>Hormonal imbalance as a contributing factor</title>
<p>Endocrine disturbances are cardinal features of MetS that may further drive LUTS pathogenesis. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.1097/01.JU.0000555000.19794.fa">Wang et&#xa0;al.</ext-link> reported that imbalances in sex steroid and insulin-like growth factor signaling have been proposed to affect prostate overgrowth and bladder dysfunction. Disentangling the precise interplay between hormones, metabolic derangements, and urinary symptomatology could unveil innovative drug targets.</p>
</sec>
<sec id="s5">
<title>Therapeutic opportunities to concurrently target MetS and LUTS</title>
<p>Recognition of the intricate associations between MetS pathologies and LUTS creates novel prospects for tailored therapeutic interventions. Lifestyle adjustments to diet and activity levels represent first-line management of MetS that could beneficially impact urinary dysfunction. Emerging drug candidates that concomitantly ameliorate metabolic abnormalities and LUTS may also hold promise. Additionally, personalized treatment regimens adapted to an individual&#x2019;s metabolic profile could optimize outcomes.</p>
</sec>
<sec id="s6">
<title>Concluding remarks</title>
<p>The recent body of evidence elucidating connections between MetS and LUTS associated with BPH and OAB has significantly advanced current comprehension of this intricate interplay. Quantitative correlations between discrete metabolic aberrations and exacerbated LUTS have been consistently demonstrated, underscoring the imperative to address metabolic factors in the management of these urologic conditions. Diverse patient cohorts and preclinical models have illuminated roles for insulin resistance, metabolic hormone disturbances, sex steroid imbalances, and chronic inflammation in the pathogenesis of MetS-related LUTS. Furthermore, modifiable lifestyle factors including dietary quality, physical activity, and smoking have emerged as major environmental contributors. Nevertheless, fully deciphering precise molecular mechanisms and causative relationships necessitates additional longitudinal clinical studies tracking MetS indices and LUTS over time, complemented by rigorously controlled animal models. By building on these research foundations, the development of innovative prevention and treatment strategies promises to dramatically improve quality of life for aging men encumbered by these burdensome urological disorders.</p>
<p>Building on the foundation laid by this compendium of research, future investigations should focus on identifying novel biomarkers for early detection and risk stratification of LUTS in the context of MetS. A deeper understanding of the genetic underpinnings of MetS-related LUTS could pave the way for personalized medicine, tailoring therapies based on individual metabolic profiles.</p>
<p>Moreover, collaborations between urologists, endocrinologists, cardiologists, and researchers from various disciplines are crucial to fully comprehend the intricate web of interactions between MetS and LUTS. These multidisciplinary efforts will accelerate the translation of scientific findings into clinically relevant applications, benefiting patients through improved diagnostics, treatment options, and patient care.</p>
<p>In addition, patient education and awareness programs must be emphasized to empower individuals to take an active role in managing their metabolic health. Addressing lifestyle factors, such as diet, physical activity, and stress management, can have a profound impact on both MetS and LUTS. Public health initiatives aimed at promoting healthier lifestyles should be encouraged to reduce the burden of MetS-related LUTS in aging populations.</p>
<p>As we make progress in better understanding the crosstalk between MetS and LUTS, it is imperative that we consider the broader societal impact. Healthcare policies and guidelines should be informed by this growing body of evidence to ensure equitable access to high-quality urological care for all individuals affected by MetS-related LUTS.</p>
<p>In conclusion, the convergence of scientific research in the fields of urology and metabolic disorders has shed light on the profound relationship between MetS and LUTS. Through concerted efforts, spanning from clinical investigations to preclinical studies and from patient education to precision medicine, we stand poised to transform the management of BPH and OAB-associated LUTS. By mitigating the encumbrance of these urological conditions through innovative prevention and treatment approaches, researchers can empower aging men to enjoy enhanced quality of life and improved health span, unfettered by the constraints imposed by MetS-related LUTS.</p>
</sec>
<sec id="s7" sec-type="author-contributions">
<title>Author contributions</title>
<p>XW: Writing &#x2013; original draft. QY: Writing &#x2013; review &amp; editing. MM: Writing &#x2013; review &amp; editing.</p>
</sec>
</body>
<back>
<sec id="s8" sec-type="funding-information">
<title>Funding</title>
<p>Work in the lab of QY was financed by grant from the National Natural Science Foundation of China (No. 81900689). Work in the lab of MM related to diabetes and other risk factors of atherosclerosis for bladder function is funded by Deutsche Forschungsgemeinschaft (Mi 294/10&#x2013;1).</p>
</sec>
<sec id="s9" 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>
<p>The authors XW, MM, QY declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.</p>
</sec>
<sec id="s10" 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>
</back>
</article>