NAD+ modulates mitochondrial vulnerability and prevents retinitis pigmentosa

NAD+ modulates mitochondrial vulnerability and prevents retinitis pigmentosa | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Article NAD+ modulates mitochondrial vulnerability and prevents retinitis pigmentosa Shaochong Zhang, Lujia Feng, Yuwen Wen, Ting Zhang, Xiaohua Zhuo, and 19 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4516112/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted You are reading this latest preprint version Abstract Retinitis pigmentosa (RP) is the most common inherited blinding retinal degenerative disease characterized by the progressive loss of photoreceptors and retinal pigment epithelium (RPE) that eventually causes retinal degeneration. However, the mechanisms that initiate RP and drive retinal vulnerability remain incompletely understood, and new strategies for its prevention and therapy are urgently needed. Mitochondrial dysfunction is the initiator of a variety of neurodegeneration, whether mitochondrial dysfunction is an important pathogenic factor of RP is still unknown. Our single-cell RNA sequencing, transmission electron microscopy, and enzyme-linked immunosorbent assay revealed that both photoreceptor cells and RPE cells of RP rats have abnormal mitochondria, accompanied by decreased levels of nicotinamide adenine dinucleotide (NAD+) metabolism which rendered the lack of NAD+ vulnerable to disease-related insults. Moreover, similar experimental results were observed in an in vitro RP model established by human primary RPE cells. Furthermore, electroretinography combined with hematoxylin-eosin, immunofluorescence analysis, and fundus photograph investigations revealed that oral administration of the NAD+ precursor nicotinamide (NMN) protected RP rats against retinal degeneration. Mechanistically, single-cell RNA sequencing, siRNA targeting, and AAV virus applications demonstrated the therapeutic effect of NMN on RP through the glyceraldehyde-phosphate dehydrogenase-mitochondria pathway. Collectively, these findings indicate that mitochondrial abnormalities may be the drivers of RP and NMN has a therapeutic effect on RP. Biological sciences/Cell biology/Mechanisms of disease Health sciences/Diseases/Eye diseases/Retinal diseases Biological sciences/Molecular biology/Transcription Full Text Additional Declarations There is NO Competing Interest. Tables 1 to 7 are available in the Supplementary Files section. Supplementary Files Table1.pdf Table 1 Table2.pdf Table 2 Table3.pdf Table 3 Table4.pdf Table 4 Table5.pdf Table 5 Table6.pdf Table 6 Table7.pdf Table 7 Cite Share Download PDF Status: Under Review Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4516112","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Article","associatedPublications":[],"authors":[{"id":319503763,"identity":"c5f3b5f2-6428-412c-b120-a74c4639807f","order_by":0,"name":"Shaochong 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pigmentosa","fulltext":[],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":false,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":true,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":true,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"nature-portfolio","isNatureJournal":true,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"","title":"Nature Portfolio","twitterHandle":"","acdcEnabled":false,"dfaEnabled":false,"editorialSystem":"ejp","reportingPortfolio":"","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-4516112/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4516112/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"Retinitis pigmentosa (RP) is the most common inherited blinding retinal degenerative disease characterized by the progressive loss of photoreceptors and retinal pigment epithelium (RPE) that eventually causes retinal degeneration. However, the mechanisms that initiate RP and drive retinal vulnerability remain incompletely understood, and new strategies for its prevention and therapy are urgently needed. Mitochondrial dysfunction is the initiator of a variety of neurodegeneration, whether mitochondrial dysfunction is an important pathogenic factor of RP is still unknown. Our single-cell RNA sequencing, transmission electron microscopy, and enzyme-linked immunosorbent assay revealed that both photoreceptor cells and RPE cells of RP rats have abnormal mitochondria, accompanied by decreased levels of nicotinamide adenine dinucleotide (NAD+) metabolism which rendered the lack of NAD+ vulnerable to disease-related insults. Moreover, similar experimental results were observed in an in vitro RP model established by human primary RPE cells. Furthermore, electroretinography combined with hematoxylin-eosin, immunofluorescence analysis, and fundus photograph investigations revealed that oral administration of the NAD+ precursor nicotinamide (NMN) protected RP rats against retinal degeneration. Mechanistically, single-cell RNA sequencing, siRNA targeting, and AAV virus applications demonstrated the therapeutic effect of NMN on RP through the glyceraldehyde-phosphate dehydrogenase-mitochondria pathway. Collectively, these findings indicate that mitochondrial abnormalities may be the drivers of RP and NMN has a therapeutic effect on RP.","manuscriptTitle":"NAD+ modulates mitochondrial vulnerability and prevents retinitis pigmentosa","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-06-28 03:30:55","doi":"10.21203/rs.3.rs-4516112/v1","editorialEvents":[],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"nature-communications","isNatureJournal":true,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"NCOMMS","sideBox":"Learn more about [Nature Communications](http://www.nature.com/ncomms/)","snPcode":"","submissionUrl":"https://mts-ncomms.nature.com/","title":"Nature Communications","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"ejp","reportingPortfolio":"Nature Communications","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"baf53da7-e30a-43d6-b622-902562141ddf","owner":[],"postedDate":"June 28th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[{"id":33782923,"name":"Biological sciences/Cell biology/Mechanisms of disease"},{"id":33782924,"name":"Health sciences/Diseases/Eye diseases/Retinal diseases"},{"id":33782925,"name":"Biological sciences/Molecular biology/Transcription"}],"tags":[],"updatedAt":"2026-04-21T06:45:28+00:00","versionOfRecord":[],"versionCreatedAt":"2024-06-28 03:30:55","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4516112","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4516112","identity":"rs-4516112","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}