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Inhibition of miR-1-3p alleviates intrauterine adhesion in rats by promoting autophagy and suppressing pyroptosis in endometrial epithelial cells through targeting Sirt3.

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Τίτλος: Inhibition of miR-1-3p alleviates intrauterine adhesion in rats by promoting autophagy and suppressing pyroptosis in endometrial epithelial cells through targeting Sirt3.
Συγγραφείς: Yan X; Department of Obstetrics & Gynecology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China., Nian L; Department of Obstetrics & Gynecology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China., Zhu L; Medical School, Kunming University of Science and Technology, Kunming 650500, China., Yan Z; Medical School, Kunming University of Science and Technology, Kunming 650500, China., Bi Y; Department of Obstetrics & Gynecology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China., Liu J; Department of Obstetrics & Gynecology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China., Ai Y; Department of Obstetrics & Gynecology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China. Electronic address: ayszfk@163.com.
Πηγή: Immunobiology [Immunobiology] 2026 Sep; Vol. 231 (5), pp. 153223. Date of Electronic Publication: 2026 Aug 03.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 8002742 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-3279 (Electronic) Linking ISSN: 01712985 NLM ISO Abbreviation: Immunobiology Subsets: MEDLINE
Imprint Name(s): Publication: <2005->: Amsterdam : Elsevier
Original Publication: Stuttgart ; New York, Fischer.
Ιατρικοί όροι (MeSH): MicroRNAs*/genetics , Pyroptosis*/genetics , Endometrium*/pathology , Endometrium*/metabolism , Epithelial Cells*/metabolism , Epithelial Cells*/pathology , Sirtuin 3*/genetics , Sirtuin 3*/metabolism, Autophagy/genetics ; Epithelial-Mesenchymal Transition/genetics ; Tissue Adhesions/genetics ; Tissue Adhesions/metabolism ; Tissue Adhesions/pathology ; Female ; Animals ; Rats ; Humans ; Disease Models, Animal ; Rats, Sprague-Dawley ; Sirtuins
Περίληψη: Background and Purpose: Intrauterine adhesion (IUA) is a prevalent gynecological disorder that causes infertility and recurrent miscarriage; however, effective treatments remain limited. This study aimed to elucidate the function of Sirt3 in IUA and explore its underlying molecular mechanisms.
Methods: A rat IUA model was established by simulating mechanical endometrial injury, and an in vitro model was induced by treating human endometrial epithelial cells (hEECs) with recombinant TGF-β1. The expression of miRNAs and key proteins was detected via RT-qPCR, Western blotting, immunohistochemistry, and immunofluorescence. Cytokine levels were measured via ELISA, and endometrial damage in rats was assessed by using hematoxylin and eosin (HE) and Masson staining.
Results: We observed significant Sirt3 downregulation in IUA. Sirt3 overexpression ameliorated endometrial damage and fibrosis in IUA rats, thereby suppressing the expression of epithelial-mesenchymal transition (EMT) markers (vimentin and N-cadherin) and fibrosis-related proteins (α-SMA and collagen I) while also restoring E-cadherin expression. The overexpression of Sirt3 could also promote autophagy in hEECs induced by TGF-β1 (which promotes the expression of LC3 and Beclin 1 and inhibits the expression of p62), inhibit pyroptosis (which suppresses the expression of caspase-1, NLRP3, GSDMD, and ASC), and downregulate the levels of IL-1β and IL-18. These effects were reversed by the autophagy inhibitor chloroquine or the pyroptosis activator nigericin. Further investigation revealed that miR-1-3p was upregulated in IUA and could directly target and negatively regulate Sirt3 expression. Treatment with miR-1-3p antagomir suppressed EMT and fibrosis in hEECs under TGF-β1 exposure; however, this effect was attenuated by concomitant Sirt3 knockdown.
Conclusion: In summary, miR-1-3p promotes IUA progression by suppressing Sirt3-mediated autophagy and activating pyroptosis, thereby driving EMT and fibrosis. The findings of this research revealed that the key role of Sirt3 in inhibiting the progression of IUA provides a potential target for the development of disease intervention therapies.
(Copyright © 2026 The Authors. Published by Elsevier GmbH.. All rights reserved.)
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Contributed Indexing: Keywords: Autophagy; Endometrial epithelial cells; Intrauterine adhesion; Pyroptosis; Sirt3; miR-1-3p
Substance Nomenclature: 0 (MicroRNAs)
EC 3.5.1.- (Sirtuin 3)
0 (SIRT3 protein, rat)
EC 3.5.1.- (Sirtuins)
Entry Date(s): Date Created: 20260810 Date Completed: 20260917 Latest Revision: 20260917
Update Code: 20260918
DOI: 10.1016/j.imbio.2026.153223
PMID: 42574784
Βάση Δεδομένων: MEDLINE
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  Data: Inhibition of miR-1-3p alleviates intrauterine adhesion in rats by promoting autophagy and suppressing pyroptosis in endometrial epithelial cells through targeting Sirt3.
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  Data: &lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Yan+X%22&quot;&gt;Yan X&lt;/searchLink&gt;; Department of Obstetrics &amp; Gynecology, The First People&#39;s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Nian+L%22&quot;&gt;Nian L&lt;/searchLink&gt;; Department of Obstetrics &amp; Gynecology, The First People&#39;s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Zhu+L%22&quot;&gt;Zhu L&lt;/searchLink&gt;; Medical School, Kunming University of Science and Technology, Kunming 650500, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Yan+Z%22&quot;&gt;Yan Z&lt;/searchLink&gt;; Medical School, Kunming University of Science and Technology, Kunming 650500, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Bi+Y%22&quot;&gt;Bi Y&lt;/searchLink&gt;; Department of Obstetrics &amp; Gynecology, The First People&#39;s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Liu+J%22&quot;&gt;Liu J&lt;/searchLink&gt;; Department of Obstetrics &amp; Gynecology, The First People&#39;s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China.&lt;br /&gt;&lt;searchLink fieldCode=&quot;AU&quot; term=&quot;%22Ai+Y%22&quot;&gt;Ai Y&lt;/searchLink&gt;; Department of Obstetrics &amp; Gynecology, The First People&#39;s Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, National Key Clinical Specialty of Gynecology, Yunnan Province Clinical Research Center for Gynecological and Obstetric Disease, Kunming 650032, China. Electronic address: ayszfk@163.com.
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– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background and Purpose: Intrauterine adhesion (IUA) is a prevalent gynecological disorder that causes infertility and recurrent miscarriage; however, effective treatments remain limited. This study aimed to elucidate the function of Sirt3 in IUA and explore its underlying molecular mechanisms.&lt;br /&gt;Methods: A rat IUA model was established by simulating mechanical endometrial injury, and an in vitro model was induced by treating human endometrial epithelial cells (hEECs) with recombinant TGF-β1. The expression of miRNAs and key proteins was detected via RT-qPCR, Western blotting, immunohistochemistry, and immunofluorescence. Cytokine levels were measured via ELISA, and endometrial damage in rats was assessed by using hematoxylin and eosin (HE) and Masson staining.&lt;br /&gt;Results: We observed significant Sirt3 downregulation in IUA. Sirt3 overexpression ameliorated endometrial damage and fibrosis in IUA rats, thereby suppressing the expression of epithelial-mesenchymal transition (EMT) markers (vimentin and N-cadherin) and fibrosis-related proteins (α-SMA and collagen I) while also restoring E-cadherin expression. The overexpression of Sirt3 could also promote autophagy in hEECs induced by TGF-β1 (which promotes the expression of LC3 and Beclin 1 and inhibits the expression of p62), inhibit pyroptosis (which suppresses the expression of caspase-1, NLRP3, GSDMD, and ASC), and downregulate the levels of IL-1β and IL-18. These effects were reversed by the autophagy inhibitor chloroquine or the pyroptosis activator nigericin. Further investigation revealed that miR-1-3p was upregulated in IUA and could directly target and negatively regulate Sirt3 expression. Treatment with miR-1-3p antagomir suppressed EMT and fibrosis in hEECs under TGF-β1 exposure; however, this effect was attenuated by concomitant Sirt3 knockdown.&lt;br /&gt;Conclusion: In summary, miR-1-3p promotes IUA progression by suppressing Sirt3-mediated autophagy and activating pyroptosis, thereby driving EMT and fibrosis. The findings of this research revealed that the key role of Sirt3 in inhibiting the progression of IUA provides a potential target for the development of disease intervention therapies.&lt;br /&gt; (Copyright &#169; 2026 The Authors. Published by Elsevier GmbH.. All rights reserved.)
– Name: Abstract
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  Data: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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  Data: &lt;i&gt;Keywords: &lt;/i&gt;Autophagy; Endometrial epithelial cells; Intrauterine adhesion; Pyroptosis; Sirt3; miR-1-3p
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        Text: English
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        StartPage: 153223
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      – SubjectFull: Autophagy genetics
        Type: general
      – SubjectFull: Epithelial-Mesenchymal Transition genetics
        Type: general
      – SubjectFull: Tissue Adhesions genetics
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        Type: general
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      – SubjectFull: MicroRNAs genetics
        Type: general
      – SubjectFull: Pyroptosis genetics
        Type: general
      – SubjectFull: Endometrium pathology
        Type: general
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      – SubjectFull: Sirtuin 3 genetics
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      – SubjectFull: Sirtuin 3 metabolism
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      – TitleFull: Inhibition of miR-1-3p alleviates intrauterine adhesion in rats by promoting autophagy and suppressing pyroptosis in endometrial epithelial cells through targeting Sirt3.
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