[{"citation":{"ama":"Goeschl V, Hotka M, Hochreiter B, et al. α-ketoglutarate dehydrogenase complex activity modulates glutamate excitotoxicity via metabotropic regulation of NMDA receptors in primary cultures. <i>Journal of Cell Science</i>. 2026;139(8). doi:<a href=\"https://doi.org/10.1242/jcs.264420\">10.1242/jcs.264420</a>","mla":"Goeschl, Vanessa, et al. “α-Ketoglutarate Dehydrogenase Complex Activity Modulates Glutamate Excitotoxicity via Metabotropic Regulation of NMDA Receptors in Primary Cultures.” <i>Journal of Cell Science</i>, vol. 139, no. 8, jcs264420, The Company of Biologists, 2026, doi:<a href=\"https://doi.org/10.1242/jcs.264420\">10.1242/jcs.264420</a>.","ieee":"V. Goeschl <i>et al.</i>, “α-ketoglutarate dehydrogenase complex activity modulates glutamate excitotoxicity via metabotropic regulation of NMDA receptors in primary cultures,” <i>Journal of Cell Science</i>, vol. 139, no. 8. The Company of Biologists, 2026.","short":"V. Goeschl, M. Hotka, B. Hochreiter, K. Hilber, S. Boehm, A.V. Kozlov, H. Kubista, Journal of Cell Science 139 (2026).","ista":"Goeschl V, Hotka M, Hochreiter B, Hilber K, Boehm S, Kozlov AV, Kubista H. 2026. α-ketoglutarate dehydrogenase complex activity modulates glutamate excitotoxicity via metabotropic regulation of NMDA receptors in primary cultures. Journal of Cell Science. 139(8), jcs264420.","chicago":"Goeschl, Vanessa, Matej Hotka, Bernhard Hochreiter, Karlheinz Hilber, Stefan Boehm, Andrey V. Kozlov, and Helmut Kubista. “α-Ketoglutarate Dehydrogenase Complex Activity Modulates Glutamate Excitotoxicity via Metabotropic Regulation of NMDA Receptors in Primary Cultures.” <i>Journal of Cell Science</i>. The Company of Biologists, 2026. <a href=\"https://doi.org/10.1242/jcs.264420\">https://doi.org/10.1242/jcs.264420</a>.","apa":"Goeschl, V., Hotka, M., Hochreiter, B., Hilber, K., Boehm, S., Kozlov, A. V., &#38; Kubista, H. (2026). α-ketoglutarate dehydrogenase complex activity modulates glutamate excitotoxicity via metabotropic regulation of NMDA receptors in primary cultures. <i>Journal of Cell Science</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/jcs.264420\">https://doi.org/10.1242/jcs.264420</a>"},"date_updated":"2026-05-12T06:40:18Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","PlanS_conform":"1","title":"α-ketoglutarate dehydrogenase complex activity modulates glutamate excitotoxicity via metabotropic regulation of NMDA receptors in primary cultures","_id":"21860","author":[{"full_name":"Goeschl, Vanessa","last_name":"Goeschl","first_name":"Vanessa"},{"full_name":"Hotka, Matej","last_name":"Hotka","first_name":"Matej"},{"full_name":"Hochreiter, Bernhard","first_name":"Bernhard","last_name":"Hochreiter","id":"e6cab3de-17f6-11ed-9210-c1e42e045e9d"},{"last_name":"Hilber","first_name":"Karlheinz","full_name":"Hilber, Karlheinz"},{"last_name":"Boehm","first_name":"Stefan","full_name":"Boehm, Stefan"},{"last_name":"Kozlov","first_name":"Andrey V.","full_name":"Kozlov, Andrey V."},{"full_name":"Kubista, Helmut","first_name":"Helmut","last_name":"Kubista"}],"date_created":"2026-05-11T10:52:27Z","status":"public","type":"journal_article","oa_version":"Published Version","article_type":"original","abstract":[{"text":"Glutamate excitotoxicity is a cell death mechanism triggered by accumulation of glutamate in the extracellular space. The α-ketoglutarate dehydrogenase complex (αKGDHC), an enzyme of the tricarboxylic acid cycle, represents a branching point controlling glutamate formation and its consumption as a fuel. Hence, modulation of the activity of αKGDHC might alter the amount of glutamate available for excitotoxic effects. To address this hypothesis, hippocampal neurons in primary co-culture with glial cells were exposed to zero-Mg2 buffer to elicit excitotoxicity through N-methyl-D-aspartic acid (NMDA) receptor disinhibition. Pretreatment of the cultures with succinyl phosphonate, to inhibit αKGDHC, enhanced excitotoxity, whereas promotion of αKGDHC activity by pretreatment with thiamine caused an opposite action. Moreover, NMDA receptor currents – but not those mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors – were potentiated in neurons with impaired αKGDHC activity and diminished in neurons with boosted αKGDHC activity. The sensitization of NMDA receptors involved mGluR1 activation and was accompanied by enhanced neuronal discharge activity, elevated basal cytosolic Ca2+ levels, and augmented Ca2+ responses evoked by glutamate application. These results suggest that mGluR1-mediated potentiation of NMDA receptors contributes to a mechanism by which inhibition of αKGDHC might exacerbate glutamate excitotoxicity.","lang":"eng"}],"OA_type":"hybrid","OA_place":"publisher","language":[{"iso":"eng"}],"publication":"Journal of Cell Science","scopus_import":"1","issue":"8","publication_identifier":{"eissn":["1477-9137"],"issn":["0021-9533"]},"acknowledgement":"The technical assistance by Tanja Wagner and Elena Lilliu is gratefully acknowledged. This research was funded in whole or in part by the Austrian Science Fund (FWF) (P36145 to H.K., PAT8605623 to M.H. and P33799 to A.V.K.]. Open Access funding provided by Medical University of Vienna and the Austrian Science Fund (FWF). Deposited in PMC for immediate release.","has_accepted_license":"1","date_published":"2026-04-27T00:00:00Z","file_date_updated":"2026-05-12T06:27:54Z","article_processing_charge":"Yes (via OA deal)","fulldoi":"https://doi.org/10.1242/jcs.264420","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"ddc":["570"],"publication_status":"published","year":"2026","quality_controlled":"1","pmid":1,"intvolume":"       139","article_number":"jcs264420","volume":139,"doi":"10.1242/jcs.264420","file":[{"access_level":"open_access","creator":"dernst","relation":"main_file","success":1,"date_created":"2026-05-12T06:27:54Z","checksum":"8db35c97588c2f6ef88c7e8d5924cf8c","file_name":"2026_JourCellScience_Goeschl.pdf","date_updated":"2026-05-12T06:27:54Z","content_type":"application/pdf","file_size":1957057,"file_id":"21861"}],"day":"27","oa":1,"external_id":{"pmid":["41834724"]},"publisher":"The Company of Biologists","month":"04","department":[{"_id":"Bio"}]},{"publication_identifier":{"eissn":["2399-3642"]},"acknowledgement":"We appreciate the technical assistance from Anna Schreilechner. We are grateful for support by all members of the animal facility team at IMB, University of Graz, as well as K. Zierler for assistance with animal licenses.  F.M, T.E., T.M., T.P., and W.F.G. are grateful to the Austrian Science Fund (FWF) for the excellence cluster 10.55776/COE14 (MetAGE), which was additionally supported by Land Styria, Stadt Graz, University of Graz and Medical University of Graz. This research was further supported by the FWF via the DKplus program 10.55776/W1226 (DK-MCD) to F.M., T.M., R.B.G., and W.F.G., 10.55776/P28529, 10.55776/I3716 (to R.M.), 10.55776/P28854, 10.55776/I3792, 10.55776/DOC130 (to T.M.), and 10.55776/I4319 (to. M.S.R.); the Austrian Research Promotion Agency (FFG) grants 864690 and 870454; the Integrative Metabolism Research Center Graz; the Austrian Infrastructure Program 2016/2017 (to T.M.), and 10.55776/COE7, 10.55776/COE17, 10.55776/FG12 and 10.55776/F73 (to R.B.G.); the Styrian Government; the City of Graz; and BioTechMed-Graz (flagship project) (to T.M.); the MEFO Graz (to W.F.G.). F.E.O., J.G. and Z.K. were doctoral fellows in the doctoral program Metabolic and Cardiovascular Disease (MCD) (FWF, 10.55776/W 1226) at the Medical University of Graz. S.v.A. and A.S. are thesis students in the excellence cluster 10.55776/COE14 (MetAGE, W.F.G.). M.H. was a fellow of the Molecular Medicine (MolMed) doctoral program at the Medical University of Graz supported by MEFO Graz. The SIM equipment is part of the Nikon Center of Excellence, Graz, and is supported by the Austrian infrastructure program 2013/ 2014, Nikon Austria Inc., and BioTechMed (to W.F.G.). Our thanks go to Shimadzu Austria for supporting this research through instrument access given in the Metabolomics and Bioprocess Analytics laboratory (TU Wien) (R.B.G.). For open access purposes, the authors have applied a CC BY public copyright license to any author-accepted manuscript version arising from this submission.” We thank the Medical University of Graz for financial support.","scopus_import":"1","publication":"Communications Biology","language":[{"iso":"eng"}],"OA_type":"gold","OA_place":"publisher","abstract":[{"text":"Presenilin-1 (PS1) is an endoplasmic reticulum protein, most known for its role in pathogenesis of familial Alzheimer’s Disease (AD). PS1 has been attributed roles in intracellular calcium homeostasis in the brain, as well as in the pancreatic beta cells, where it has been shown to be fundamental for the initial phase of glucose-induced insulin secretion. To gain mechanistic insight into beta cell autonomous function of PS1, we have examined various beta cell models and found that PS1 controls glycolytic flux of pancreatic beta cells by regulating sub-mitochondrial Ca2+ homeostasis. Transient knock down of PS1 yielded a glycolytic bottleneck at the step catalyzed by glyceraldehyde-3-phosphate dehydrogenase, resulting in defective glucose responsiveness. Moreover, we show that PS1 is needed for the preservation of beta cell identity, likely due to its role in glycolysis. Finally, we show that mouse islets from an in vivo model of AD mimic the defective glucose responsiveness seen in beta cells with transient PS1 knock down, while the identity loss and whole-body glucose homeostasis are not severely impacted, suggesting an adaptive response. Thus, the current work highlights beta cell autonomous role of PS1 and adds a layer of complexity in its impact on whole body metabolism.","lang":"eng"}],"oa_version":"Published Version","type":"journal_article","article_type":"original","status":"public","date_created":"2026-10-18T22:01:50Z","author":[{"full_name":"Koshenov, Zhanat","first_name":"Zhanat","last_name":"Koshenov"},{"first_name":"Sandra","last_name":"Postic","full_name":"Postic, Sandra"},{"last_name":"Schoiswohl","first_name":"Gabriela","full_name":"Schoiswohl, Gabriela"},{"full_name":"Van Amsterdam, Savina","last_name":"Van Amsterdam","first_name":"Savina"},{"full_name":"Hois-Zelinka, Victoria","first_name":"Victoria","last_name":"Hois-Zelinka"},{"last_name":"Oflaz","first_name":"Furkan E.","full_name":"Oflaz, Furkan E."},{"full_name":"Rost, Rene","first_name":"Rene","last_name":"Rost"},{"full_name":"Tiapko, Oleksandra","first_name":"Oleksandra","last_name":"Tiapko"},{"full_name":"Gottschalk, Benjamin","last_name":"Gottschalk","first_name":"Benjamin"},{"full_name":"Hirtl, Martin","last_name":"Hirtl","first_name":"Martin"},{"full_name":"Bachkoenig, Olaf G.","last_name":"Bachkoenig","first_name":"Olaf G."},{"last_name":"Koshenova","first_name":"Aigerim","full_name":"Koshenova, Aigerim"},{"full_name":"Erdogan, Yusuf C.","first_name":"Yusuf C.","last_name":"Erdogan"},{"first_name":"Adlet","last_name":"Sagintayev","full_name":"Sagintayev, Adlet"},{"first_name":"Anita","last_name":"Krnjic","full_name":"Krnjic, Anita"},{"last_name":"Pfabe","first_name":"Johannes U.","full_name":"Pfabe, Johannes U."},{"id":"35F0286E-F248-11E8-B48F-1D18A9856A87","first_name":"Srdjan","last_name":"Sarikas","full_name":"Sarikas, Srdjan"},{"id":"e6cab3de-17f6-11ed-9210-c1e42e045e9d","last_name":"Hochreiter","first_name":"Bernhard","full_name":"Hochreiter, Bernhard"},{"first_name":"Juergen","last_name":"Gindlhuber","full_name":"Gindlhuber, Juergen"},{"first_name":"Matthias","last_name":"Schittmayer","full_name":"Schittmayer, Matthias"},{"first_name":"Jelena","last_name":"Tadic","full_name":"Tadic, Jelena"},{"full_name":"Ehall, Barbara","first_name":"Barbara","last_name":"Ehall"},{"full_name":"Madeo, Frank","last_name":"Madeo","first_name":"Frank"},{"first_name":"Tobias","last_name":"Madl","full_name":"Madl, Tobias"},{"first_name":"Roland","last_name":"Malli","full_name":"Malli, Roland"},{"first_name":"Ruth","last_name":"Birner-Gruenberger","full_name":"Birner-Gruenberger, Ruth"},{"last_name":"Pieber","first_name":"Thomas","full_name":"Pieber, Thomas"},{"first_name":"Tobias","last_name":"Eisenberg","full_name":"Eisenberg, Tobias"},{"full_name":"Slak Rupnik, Marjan","last_name":"Slak Rupnik","first_name":"Marjan"},{"full_name":"Graier, Wolfgang F.","last_name":"Graier","first_name":"Wolfgang F."}],"title":"Presenilin-1 controls glycolysis and identity of pancreatic beta cells","_id":"23148","PlanS_conform":"1","supplementarymaterial":"yes","date_updated":"2026-10-19T06:23:26Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Koshenov, Zhanat, Sandra Postic, Gabriela Schoiswohl, Savina Van Amsterdam, Victoria Hois-Zelinka, Furkan E. Oflaz, Rene Rost, et al. “Presenilin-1 Controls Glycolysis and Identity of Pancreatic Beta Cells.” <i>Communications Biology</i>. Springer Nature, 2026. <a href=\"https://doi.org/10.1038/s42003-026-10581-6\">https://doi.org/10.1038/s42003-026-10581-6</a>.","apa":"Koshenov, Z., Postic, S., Schoiswohl, G., Van Amsterdam, S., Hois-Zelinka, V., Oflaz, F. E., … Graier, W. F. (2026). Presenilin-1 controls glycolysis and identity of pancreatic beta cells. <i>Communications Biology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s42003-026-10581-6\">https://doi.org/10.1038/s42003-026-10581-6</a>","ama":"Koshenov Z, Postic S, Schoiswohl G, et al. Presenilin-1 controls glycolysis and identity of pancreatic beta cells. <i>Communications Biology</i>. 2026;9. doi:<a href=\"https://doi.org/10.1038/s42003-026-10581-6\">10.1038/s42003-026-10581-6</a>","mla":"Koshenov, Zhanat, et al. “Presenilin-1 Controls Glycolysis and Identity of Pancreatic Beta Cells.” <i>Communications Biology</i>, vol. 9, 1315, Springer Nature, 2026, doi:<a href=\"https://doi.org/10.1038/s42003-026-10581-6\">10.1038/s42003-026-10581-6</a>.","short":"Z. Koshenov, S. Postic, G. Schoiswohl, S. Van Amsterdam, V. Hois-Zelinka, F.E. Oflaz, R. Rost, O. Tiapko, B. Gottschalk, M. Hirtl, O.G. Bachkoenig, A. Koshenova, Y.C. Erdogan, A. Sagintayev, A. Krnjic, J.U. Pfabe, S. Sarikas, B. Hochreiter, J. Gindlhuber, M. Schittmayer, J. Tadic, B. Ehall, F. Madeo, T. Madl, R. Malli, R. Birner-Gruenberger, T. Pieber, T. Eisenberg, M. Slak Rupnik, W.F. Graier, Communications Biology 9 (2026).","ista":"Koshenov Z, Postic S, Schoiswohl G, Van Amsterdam S, Hois-Zelinka V, Oflaz FE, Rost R, Tiapko O, Gottschalk B, Hirtl M, Bachkoenig OG, Koshenova A, Erdogan YC, Sagintayev A, Krnjic A, Pfabe JU, Sarikas S, Hochreiter B, Gindlhuber J, Schittmayer M, Tadic J, Ehall B, Madeo F, Madl T, Malli R, Birner-Gruenberger R, Pieber T, Eisenberg T, Slak Rupnik M, Graier WF. 2026. Presenilin-1 controls glycolysis and identity of pancreatic beta cells. Communications Biology. 9, 1315.","ieee":"Z. Koshenov <i>et al.</i>, “Presenilin-1 controls glycolysis and identity of pancreatic beta cells,” <i>Communications Biology</i>, vol. 9. Springer Nature, 2026."},"DOAJ_listed":"1","publisher":"Springer Nature","month":"10","department":[{"_id":"FISS"}],"external_id":{"pmid":["42387039"]},"oa":1,"day":"08","dataavailabilitystatement":"The data supporting the findings of this research can be obtained from the authors upon a reasonable request; please refer to the author’s contributions for details regarding specific datasets. Numerical source data underlying graphs in this article can be found in Supplementary data file. Supplementary Figs. and figure legends are included in the Supplementary file. The code used in this study is available from the authors on reasonable request.","doi":"10.1038/s42003-026-10581-6","researchdata_availability":"upon request","file":[{"file_id":"23161","file_size":1819866,"content_type":"application/pdf","date_updated":"2026-10-19T06:19:39Z","file_name":"2026_CommunicationsBiology_Koshenov.pdf","date_created":"2026-10-19T06:19:39Z","checksum":"b90e60a625fcac8ef5d9ff968792d675","success":1,"relation":"main_file","creator":"dernst","access_level":"open_access"}],"volume":9,"article_number":"1315","intvolume":"         9","publication_status":"published","quality_controlled":"1","year":"2026","pmid":1,"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"ddc":["570"],"das_tickbox":"1","fulldoi":"https://doi.org/10.1038/s42003-026-10581-6","article_processing_charge":"Yes","has_accepted_license":"1","date_published":"2026-10-08T00:00:00Z","file_date_updated":"2026-10-19T06:19:39Z"},{"date_created":"2025-12-29T12:16:22Z","author":[{"last_name":"Stopa","first_name":"Victoria","full_name":"Stopa, Victoria"},{"first_name":"Miron","last_name":"Sopić","full_name":"Sopić, Miron"},{"full_name":"Li, Guanliang","last_name":"Li","first_name":"Guanliang"},{"full_name":"Sluimer, Judith","last_name":"Sluimer","first_name":"Judith"},{"last_name":"Basílio","first_name":"José","full_name":"Basílio, José"},{"last_name":"van der Laan","first_name":"Sander W.","full_name":"van der Laan, Sander W."},{"full_name":"Kreil, David P.","first_name":"David P.","last_name":"Kreil"},{"full_name":"Devaux, Yvan","last_name":"Devaux","first_name":"Yvan"},{"full_name":"Hochreiter, Bernhard","last_name":"Hochreiter","first_name":"Bernhard","id":"e6cab3de-17f6-11ed-9210-c1e42e045e9d"}],"status":"public","title":"Essentials of transcriptomic methods: Navigating through RNA sequencing and beyond","editor":[{"full_name":"Devaux, Yvan","first_name":"Yvan","last_name":"Devaux"},{"last_name":"Sopic","first_name":"Miron","full_name":"Sopic, Miron"}],"_id":"20870","abstract":[{"lang":"eng","text":"RNA sequencing (RNA-seq) methodologies have evolved rapidly, offering powerful tools to study gene expression, transcriptome dynamics, and molecular mechanisms in various biological contexts. However, the complexity of these approaches poses challenges in data interpretation, sensitivity, and applicability. This chapter provides a comprehensive overview of RNA-seq methodologies, highlighting their advantages, limitations, and applications, particularly in cardiovascular research. Bulk RNA sequencing enables high-throughput gene expression profiling but lacks the resolution to capture cellular heterogeneity and spatial context. Direct RNA sequencing preserves native RNA modifications, offering insights into post-transcriptional regulation, though it remains technically challenging. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) bridge these gaps by resolving transcriptomic complexity at the cellular level and within tissue architecture, providing crucial insights into disease mechanisms such as atherosclerosis. By summarizing the strengths and limitations of these methodologies, this chapter aims to guide researchers in selecting the most suitable transcriptomic approach for their studies, ultimately advancing precision medicine and biomarker discovery in cardiovascular disease."}],"type":"book_chapter","publication_status":"published","oa_version":"None","quality_controlled":"1","year":"2025","page":"131-172","citation":{"apa":"Stopa, V., Sopić, M., Li, G., Sluimer, J., Basílio, J., van der Laan, S. W., … Hochreiter, B. (2025). Essentials of transcriptomic methods: Navigating through RNA sequencing and beyond. In Y. Devaux &#38; M. Sopic (Eds.), <i>Transcriptomics in Atherosclerosis</i> (pp. 131–172). Elsevier. <a href=\"https://doi.org/10.1016/b978-0-443-33064-3.00016-5\">https://doi.org/10.1016/b978-0-443-33064-3.00016-5</a>","chicago":"Stopa, Victoria, Miron Sopić, Guanliang Li, Judith Sluimer, José Basílio, Sander W. van der Laan, David P. Kreil, Yvan Devaux, and Bernhard Hochreiter. “Essentials of Transcriptomic Methods: Navigating through RNA Sequencing and Beyond.” In <i>Transcriptomics in Atherosclerosis</i>, edited by Yvan Devaux and Miron Sopic, 131–72. Elsevier, 2025. <a href=\"https://doi.org/10.1016/b978-0-443-33064-3.00016-5\">https://doi.org/10.1016/b978-0-443-33064-3.00016-5</a>.","short":"V. Stopa, M. Sopić, G. Li, J. Sluimer, J. Basílio, S.W. van der Laan, D.P. Kreil, Y. Devaux, B. Hochreiter, in:, Y. Devaux, M. Sopic (Eds.), Transcriptomics in Atherosclerosis, Elsevier, 2025, pp. 131–172.","ieee":"V. Stopa <i>et al.</i>, “Essentials of transcriptomic methods: Navigating through RNA sequencing and beyond,” in <i>Transcriptomics in Atherosclerosis</i>, Y. Devaux and M. Sopic, Eds. Elsevier, 2025, pp. 131–172.","ista":"Stopa V, Sopić M, Li G, Sluimer J, Basílio J, van der Laan SW, Kreil DP, Devaux Y, Hochreiter B. 2025.Essentials of transcriptomic methods: Navigating through RNA sequencing and beyond. In: Transcriptomics in Atherosclerosis. , 131–172.","mla":"Stopa, Victoria, et al. “Essentials of Transcriptomic Methods: Navigating through RNA Sequencing and Beyond.” <i>Transcriptomics in Atherosclerosis</i>, edited by Yvan Devaux and Miron Sopic, Elsevier, 2025, pp. 131–72, doi:<a href=\"https://doi.org/10.1016/b978-0-443-33064-3.00016-5\">10.1016/b978-0-443-33064-3.00016-5</a>.","ama":"Stopa V, Sopić M, Li G, et al. Essentials of transcriptomic methods: Navigating through RNA sequencing and beyond. In: Devaux Y, Sopic M, eds. <i>Transcriptomics in Atherosclerosis</i>. Elsevier; 2025:131-172. doi:<a href=\"https://doi.org/10.1016/b978-0-443-33064-3.00016-5\">10.1016/b978-0-443-33064-3.00016-5</a>"},"article_processing_charge":"No","date_published":"2025-10-24T00:00:00Z","date_updated":"2026-01-05T11:49:54Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","fulldoi":"https://doi.org/10.1016/b978-0-443-33064-3.00016-5","scopus_import":"1","publication":"Transcriptomics in Atherosclerosis","day":"24","publisher":"Elsevier","month":"10","publication_identifier":{"isbn":["9780443330643"]},"department":[{"_id":"Bio"}],"OA_type":"closed access","doi":"10.1016/b978-0-443-33064-3.00016-5","language":[{"iso":"eng"}]}]