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This study examined whether maximal elastance (mE) reliably and validly assesses bladder contractility\n                      <jats:italic>in vivo<\/jats:italic>\n                      and investigated the role of myostatin\u2010associated tissue remodelling in the contractility deficits in diabetic bladder. Eighty\u2010three female Sprague\u2013Dawley rats were assigned to control (CON), streptozotocin\u2010treated (STZ; 30\u00a0mg\/kg twice,\n                      <jats:sc>i.p.<\/jats:sc>\n                      ) and STZ with non\u2010specific IgG (STZ\u00a0+\u00a0IgG; 2\u00a0mg\/kg,\n                      <jats:sc>i.p.<\/jats:sc>\n                      ) or Myo\u2010029 (a myostatin\u2010neutralizing antibody; STZ\u00a0+\u00a0MYO; 2\u00a0mg\/kg,\n                      <jats:sc>i.p.<\/jats:sc>\n                      ). The slope of the end\u2010emission pressure\u2013volume relationship obtained from pressure\u2013volume analysis was calculated as mE. mE remained relatively constant under altered preload and afterload but increased dose dependently with muscarine infusion (10 and 100 \u00b5M, 0.002\u00a0mL\/min,\n                      <jats:sc>i.a.<\/jats:sc>\n                      ) and decreased with atropine infusion (10 and 100 \u00b5M, 0.002\u00a0mL\/min,\n                      <jats:sc>i.a.<\/jats:sc>\n                      ). Compared to CON the STZ group showed decreased mE, reduced muscle\u2010to\u2010collagen ratio, increased myostatin expression, decreased myosin heavy chain 11 (MHC 11) and smoothelin expressions, as well as upregulated \u03b1\u2010smooth muscle actin (SMA) and collagen type I alpha 1 (COL1A1) expressions. Treatment with Myo\u2010029 in STZ animals reversed the reductions in the MHC 11 and smoothelin expressions, muscle\u2010to\u2010collagen ratio and mE, as well as the STZ\u2010upregulated SMA and COL1A1 expression. Collectively mE effectively assessed bladder contractility\n                      <jats:italic>in vivo<\/jats:italic>\n                      . Moreover myostatin contributes to diabetes\u2010associated deficits in bladder contractility by regulating detrusor remodelling, suggesting that myostatin may represent a potential therapeutic target for diabetes\u2010associated cystopathy.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70838-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Developing a methodology capable of precisely assessing bladder contractility\n                            <jats:italic>in vivo<\/jats:italic>\n                            is warranted to elucidate the underlying pathophysiology of bladder contractility impairments.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The pathological progression of diabetic cystopathy has been linked to myogenic dysfunction of the detrusor, resulting in impaired bladder contractility.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Maximal elastance (mE) is a bladder contractility\u2013sensitive parameter that is independent of bladder preload and afterload.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Bladders from long\u2010standing diabetic rats exhibit diminished contractility, accompanied by upregulation of myostatin and downregulation of myosin heavy chain 11 and smoothelin.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Administration of a myostatin\u2010specific neutralizing antibody in diabetic rats reversed diabetes\u2010associated downregulation of myosin heavy chain 11 and smoothelin, as well as bladder contractility impairment.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            mE effectively assessed bladder contractility\n                            <jats:italic>in vivo<\/jats:italic>\n                            . Moreover myostatin contributes to diabetes\u2010associated deficits in bladder contractility by regulating myostatin\u2010dependent detrusor remodelling, suggesting that myostatin may represent a potential therapeutic target for diabetic cystopathy.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp291025","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T17:27:22Z","timestamp":1789752442000},"page":"8428-8449","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Myostatin\u2010dependent detrusor remodelling mediates contractility impairment in diabetic rats\u2019 bladder \u2013 a maximal elastance analysis"],"prefix":"10.1113","volume":"604","author":[{"given":"Cheng\u2010Yuan","family":"Lai","sequence":"first","affiliation":[{"name":"Institute of Biomedical Sciences Mackay Medical College  New Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui\u2010Hsuan","family":"Lau","sequence":"additional","affiliation":[{"name":"Department of Medicine Mackay Medical College  New Taipei Taiwan"},{"name":"Division of Urogynecology, Department of Obstetrics and Gynecology Mackay Memorial Hospital  Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming\u2010Chun","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Department of Medicine Mackay Medical College  New Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsien\u2010Yu","family":"Peng","sequence":"additional","affiliation":[{"name":"Department of Medicine Mackay Medical College  New Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dylan","family":"Chou","sequence":"additional","affiliation":[{"name":"Department of Medicine Mackay Medical College  New Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsung\u2010Hsien","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Medicine Mackay Medical College  New Taipei Taiwan"},{"name":"Division of Urogynecology, Department of Obstetrics and Gynecology Mackay Memorial Hospital  Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tzer\u2010Bin","family":"Lin","sequence":"additional","affiliation":[{"name":"Institute of Translational Medicine and New Drug Development, College of Medicine China Medical University  Taichung Taiwan"},{"name":"Department of Physiology, School of Medicine, College of Medicine Taipei Medical University  Taipei Taiwan"},{"name":"Graduate Institute of Biomedical Electronics and Bioinformatics National Taiwan University  Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,18]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1442-2042.2008.02052.x"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(22)01655-5"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.urology.2010.04.062"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1155\/2021\/6644631"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2005.08.027"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.28.1.177"},{"issue":"6","key":"e_1_2_6_8_1","first-page":"S18","article-title":"Diabetic bladder 543 dysfunction: Current translational knowledge","volume":"182","author":"Daneshgari F.","year":"2009","journal-title":"Journal D Urologie"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1159\/000358728"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199309303291401"},{"issue":"1","key":"e_1_2_6_11_1","article-title":"Evaluation of urodynamic pattern in short and long\u2010standing diabetic patients","volume":"95","author":"Elsakka H.","year":"2023","journal-title":"Archivio Italiano Di Urologia, Andrologia"},{"key":"e_1_2_6_12_1","unstructured":"Frank O.(1897).Die wirkung von Digitalis (Helleborein) auf das herz. 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