Noncoding RNA as a crucial epigenetic modulator in the degeneration of the ligamentum flavum
Ligamentum flavum degeneration, including hypertrophy and ossification of the ligamentum flavum, leads to degenerative spinal stenosis in older adults. However, the underlying mechanisms of ligamentum flavum degeneration remain unclear, and therapeutic strategies are limited. Noncoding RNAs include...
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description | Ligamentum flavum degeneration, including hypertrophy and ossification of the ligamentum flavum, leads to degenerative spinal stenosis in older adults. However, the underlying mechanisms of ligamentum flavum degeneration remain unclear, and therapeutic strategies are limited. Noncoding RNAs include microRNAs, circular RNAs, and long noncoding RNAs. As important epigenetic modifications, noncoding RNAs are involved in the progression of several age-related diseases, including ligamentum flavum degeneration. Previous studies have shown that noncoding RNAs can regulate the osteogenic differentiation and fibrosis of ligamentum flavum cells by regulating the expression of related genes. In this review, we discuss noncoding RNAs and their role in ligamentum flavum degeneration.
Understanding non-coding RNAs in spinal stenosis
Degenerative Spinal Stenosis (DSS), a common condition in older adults causing numbness and muscle weakness, is often caused by the breakdown of the ligamentum flavum, a spinal structure. Despite DSS’s commonness, the role of non-coding RNAs, molecules that don’t code for proteins but regulate gene activity, in LF breakdown is not well understood. Researchers reviewed the biological functions of ncRNAs in LF breakdown, focusing on microRNAs, circular RNAs, and long non-coding RNAs, aiming to provide new insights. They identified specific ncRNAs contributing to LF degeneration, suggesting their potential as treatment targets. This research could guide future studies towards non-surgical treatments for DSS. The findings reveal that manipulating these ncRNAs could offer new treatment options. This could lead to targeted therapies addressing DSS’s underlying causes, offering hope for less invasive treatments in the future.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. |
doi_str_mv | 10.1038/s12276-024-01348-2 |
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Understanding non-coding RNAs in spinal stenosis
Degenerative Spinal Stenosis (DSS), a common condition in older adults causing numbness and muscle weakness, is often caused by the breakdown of the ligamentum flavum, a spinal structure. Despite DSS’s commonness, the role of non-coding RNAs, molecules that don’t code for proteins but regulate gene activity, in LF breakdown is not well understood. Researchers reviewed the biological functions of ncRNAs in LF breakdown, focusing on microRNAs, circular RNAs, and long non-coding RNAs, aiming to provide new insights. They identified specific ncRNAs contributing to LF degeneration, suggesting their potential as treatment targets. This research could guide future studies towards non-surgical treatments for DSS. The findings reveal that manipulating these ncRNAs could offer new treatment options. This could lead to targeted therapies addressing DSS’s underlying causes, offering hope for less invasive treatments in the future.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.</description><identifier>ISSN: 2092-6413</identifier><identifier>ISSN: 1226-3613</identifier><identifier>EISSN: 2092-6413</identifier><identifier>DOI: 10.1038/s12276-024-01348-2</identifier><identifier>PMID: 39617784</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/80/509 ; 692/698/1671/1600 ; Age ; Animals ; Artificial intelligence ; Biomedical and Life Sciences ; Biomedicine ; Cell differentiation ; Circular RNA ; Degeneration ; Epigenesis, Genetic ; Epigenetics ; Fibrosis ; Gene Expression Regulation ; Humans ; Hypertrophy ; Ligamentum Flavum - metabolism ; Ligamentum Flavum - pathology ; Medical Biochemistry ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; Molecular Medicine ; Non-coding RNA ; Older people ; Ossification ; Review ; Review Article ; RNA, Circular - genetics ; RNA, Untranslated - genetics ; Spinal stenosis ; Stem Cells ; 생화학</subject><ispartof>Experimental and Molecular Medicine, 2024, 56(0), , pp.2551-2558</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>Copyright Springer Nature B.V. Dec 2024</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c457t-44bdf5ad51640f369972b72747f311999a13e72972ce7e82eefb31cdfd0cde33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671540/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671540/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39617784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART003159393$$DAccess content in National Research Foundation of Korea (NRF)$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Yongzhao</creatorcontrib><creatorcontrib>Xiang, Qian</creatorcontrib><creatorcontrib>Tian, Shuo</creatorcontrib><creatorcontrib>Wu, Zhenquan</creatorcontrib><creatorcontrib>Lin, Jialiang</creatorcontrib><creatorcontrib>Wang, Longjie</creatorcontrib><creatorcontrib>Sun, Zhuoran</creatorcontrib><creatorcontrib>Li, Weishi</creatorcontrib><title>Noncoding RNA as a crucial epigenetic modulator in the degeneration of the ligamentum flavum</title><title>Experimental & molecular medicine</title><addtitle>Exp Mol Med</addtitle><addtitle>Exp Mol Med</addtitle><description>Ligamentum flavum degeneration, including hypertrophy and ossification of the ligamentum flavum, leads to degenerative spinal stenosis in older adults. However, the underlying mechanisms of ligamentum flavum degeneration remain unclear, and therapeutic strategies are limited. Noncoding RNAs include microRNAs, circular RNAs, and long noncoding RNAs. As important epigenetic modifications, noncoding RNAs are involved in the progression of several age-related diseases, including ligamentum flavum degeneration. Previous studies have shown that noncoding RNAs can regulate the osteogenic differentiation and fibrosis of ligamentum flavum cells by regulating the expression of related genes. In this review, we discuss noncoding RNAs and their role in ligamentum flavum degeneration.
Understanding non-coding RNAs in spinal stenosis
Degenerative Spinal Stenosis (DSS), a common condition in older adults causing numbness and muscle weakness, is often caused by the breakdown of the ligamentum flavum, a spinal structure. Despite DSS’s commonness, the role of non-coding RNAs, molecules that don’t code for proteins but regulate gene activity, in LF breakdown is not well understood. Researchers reviewed the biological functions of ncRNAs in LF breakdown, focusing on microRNAs, circular RNAs, and long non-coding RNAs, aiming to provide new insights. They identified specific ncRNAs contributing to LF degeneration, suggesting their potential as treatment targets. This research could guide future studies towards non-surgical treatments for DSS. The findings reveal that manipulating these ncRNAs could offer new treatment options. This could lead to targeted therapies addressing DSS’s underlying causes, offering hope for less invasive treatments in the future.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.</description><subject>631/80/509</subject><subject>692/698/1671/1600</subject><subject>Age</subject><subject>Animals</subject><subject>Artificial intelligence</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell differentiation</subject><subject>Circular RNA</subject><subject>Degeneration</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Ligamentum Flavum - metabolism</subject><subject>Ligamentum Flavum - pathology</subject><subject>Medical Biochemistry</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Molecular Medicine</subject><subject>Non-coding RNA</subject><subject>Older people</subject><subject>Ossification</subject><subject>Review</subject><subject>Review Article</subject><subject>RNA, Circular - 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metabolism</topic><topic>Ligamentum Flavum - pathology</topic><topic>Medical Biochemistry</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Molecular Medicine</topic><topic>Non-coding RNA</topic><topic>Older people</topic><topic>Ossification</topic><topic>Review</topic><topic>Review Article</topic><topic>RNA, Circular - genetics</topic><topic>RNA, Untranslated - genetics</topic><topic>Spinal stenosis</topic><topic>Stem Cells</topic><topic>생화학</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Yongzhao</creatorcontrib><creatorcontrib>Xiang, Qian</creatorcontrib><creatorcontrib>Tian, Shuo</creatorcontrib><creatorcontrib>Wu, Zhenquan</creatorcontrib><creatorcontrib>Lin, Jialiang</creatorcontrib><creatorcontrib>Wang, Longjie</creatorcontrib><creatorcontrib>Sun, Zhuoran</creatorcontrib><creatorcontrib>Li, Weishi</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><collection>Korean Citation Index</collection><jtitle>Experimental & molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Yongzhao</au><au>Xiang, Qian</au><au>Tian, Shuo</au><au>Wu, Zhenquan</au><au>Lin, Jialiang</au><au>Wang, Longjie</au><au>Sun, Zhuoran</au><au>Li, Weishi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Noncoding RNA as a crucial epigenetic modulator in the degeneration of the ligamentum flavum</atitle><jtitle>Experimental & molecular medicine</jtitle><stitle>Exp Mol Med</stitle><addtitle>Exp Mol Med</addtitle><date>2024-12-01</date><risdate>2024</risdate><volume>56</volume><issue>12</issue><spage>2551</spage><epage>2558</epage><pages>2551-2558</pages><issn>2092-6413</issn><issn>1226-3613</issn><eissn>2092-6413</eissn><abstract>Ligamentum flavum degeneration, including hypertrophy and ossification of the ligamentum flavum, leads to degenerative spinal stenosis in older adults. However, the underlying mechanisms of ligamentum flavum degeneration remain unclear, and therapeutic strategies are limited. Noncoding RNAs include microRNAs, circular RNAs, and long noncoding RNAs. As important epigenetic modifications, noncoding RNAs are involved in the progression of several age-related diseases, including ligamentum flavum degeneration. Previous studies have shown that noncoding RNAs can regulate the osteogenic differentiation and fibrosis of ligamentum flavum cells by regulating the expression of related genes. In this review, we discuss noncoding RNAs and their role in ligamentum flavum degeneration.
Understanding non-coding RNAs in spinal stenosis
Degenerative Spinal Stenosis (DSS), a common condition in older adults causing numbness and muscle weakness, is often caused by the breakdown of the ligamentum flavum, a spinal structure. Despite DSS’s commonness, the role of non-coding RNAs, molecules that don’t code for proteins but regulate gene activity, in LF breakdown is not well understood. Researchers reviewed the biological functions of ncRNAs in LF breakdown, focusing on microRNAs, circular RNAs, and long non-coding RNAs, aiming to provide new insights. They identified specific ncRNAs contributing to LF degeneration, suggesting their potential as treatment targets. This research could guide future studies towards non-surgical treatments for DSS. The findings reveal that manipulating these ncRNAs could offer new treatment options. This could lead to targeted therapies addressing DSS’s underlying causes, offering hope for less invasive treatments in the future.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>39617784</pmid><doi>10.1038/s12276-024-01348-2</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/80/509 692/698/1671/1600 Age Animals Artificial intelligence Biomedical and Life Sciences Biomedicine Cell differentiation Circular RNA Degeneration Epigenesis, Genetic Epigenetics Fibrosis Gene Expression Regulation Humans Hypertrophy Ligamentum Flavum - metabolism Ligamentum Flavum - pathology Medical Biochemistry MicroRNAs MicroRNAs - genetics miRNA Molecular Medicine Non-coding RNA Older people Ossification Review Review Article RNA, Circular - genetics RNA, Untranslated - genetics Spinal stenosis Stem Cells 생화학 |
title | Noncoding RNA as a crucial epigenetic modulator in the degeneration of the ligamentum flavum |
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