{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:54:56Z","timestamp":1791996896280,"version":"4.4.0"},"reference-count":80,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,3]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202503000-00032\/figure1\/v\/2026-05-05T095626Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>\n                    Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Sal) is a catechol isoquinoline that causes neurotoxicity and shares structural similarity with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, an environmental toxin that causes Parkinson\u2019s disease. However, the mechanism by which Sal mediates dopaminergic neuronal death remains unclear. In this study, we found that Sal significantly enhanced the global level of N\n                    <jats:sup>6<\/jats:sup>\n                    -methyladenosine (m\n                    <jats:sup>6<\/jats:sup>\n                    A) RNA methylation in PC12 cells, mainly by inducing the downregulation of the expression of m\n                    <jats:sup>6<\/jats:sup>\n                    A demethylases fat mass and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5). RNA sequencing analysis showed that Sal downregulated the Hippo signaling pathway. The m\n                    <jats:sup>6<\/jats:sup>\n                    A reader YTH domain-containing family protein 2 (YTHDF2) promoted the degradation of m\n                    <jats:sup>6<\/jats:sup>\n                    A-containing Yes-associated protein 1 (\n                    <jats:italic toggle=\"yes\">YAP1<\/jats:italic>\n                    ) mRNA, which is a downstream key effector in the Hippo signaling pathway. Additionally, downregulation of YAP1 promoted autophagy, indicating that the mutual regulation between YAP1 and autophagy can lead to neurotoxicity. These findings reveal the role of Sal on m\n                    <jats:sup>6<\/jats:sup>\n                    A RNA methylation and suggest that Sal may act as an RNA methylation inducer mediating dopaminergic neuronal death through YAP1 and autophagy. Our results provide greater insights into the neurotoxic effects of catechol isoquinolines compared with other studies and may be a reference for assessing the involvement of RNA methylation in the pathogenesis of Parkinson\u2019s disease.\n                  <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-23-01592","type":"journal-article","created":{"date-parts":[[2024,6,18]],"date-time":"2024-06-18T01:04:13Z","timestamp":1718672653000},"page":"887-899","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":13,"title":["Salsolinol as an RNA m6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy"],"prefix":"10.4103","volume":"20","author":[{"given":"Jianan","family":"Wang","sequence":"first","affiliation":[{"name":"Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life, Beijing University of Technology, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanyuan","family":"Ran","sequence":"additional","affiliation":[{"name":"Department of Rehabilitation, Beijing Rehabilitation Hospital, Capital Medical University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zihan","family":"Li","sequence":"additional","affiliation":[{"name":"Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life, Beijing University of Technology, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianyuan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life, Beijing University of Technology, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fangfang","family":"Zhang","sequence":"additional","affiliation":[{"name":"Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life, Beijing University of Technology, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-9208-7985","authenticated-orcid":false,"given":"Juan","family":"Wang","sequence":"additional","affiliation":[{"name":"Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life, Beijing University of Technology, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4685-1057","authenticated-orcid":false,"given":"Zongjian","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Rehabilitation, Beijing Rehabilitation Hospital, Capital Medical University, Beijing, 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