{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T11:25:41Z","timestamp":1788175541888,"version":"build-2803163510"},"reference-count":70,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"13","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2024,9,24]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Cardiomyocyte growth is coupled with active protein synthesis, which is one of the basic biological processes in living cells. However, it is unclear whether the unfolded protein response transducers and effectors directly take part in the control of protein synthesis. The connection between critical functions of the unfolded protein response in cellular physiology and requirements of multiple processes for cell growth prompted us to investigate the role of the unfolded protein response in cell growth and underlying molecular mechanisms.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>Cardiomyocyte-specific inositol-requiring enzyme 1\u03b1 (IRE1\u03b1) knockout and overexpression mouse models were generated to explore its function in vivo. Neonatal rat ventricular myocytes were isolated and cultured to evaluate the role of IRE1\u03b1 in cardiomyocyte growth in vitro. Mass spectrometry was conducted to identify novel interacting proteins of IRE1\u03b1. Ribosome sequencing and polysome profiling were performed to determine the molecular basis for the function of IRE1\u03b1 in translational control.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>We show that IRE1\u03b1 is required for cell growth in neonatal rat ventricular myocytes under prohypertrophy treatment and in HEK293 cells in response to serum stimulation. At the molecular level, IRE1\u03b1 directly interacts with eIF4G and eIF3, 2 critical components of the translation initiation complex. We demonstrate that IRE1\u03b1 facilitates the formation of the translation initiation complex around the endoplasmic reticulum and preferentially initiates the translation of transcripts with 5\u2019 terminal oligopyrimidine motifs. We then reveal that IRE1\u03b1 plays an important role in determining the selectivity and translation of these transcripts. We next show that IRE1\u03b1 stimulates the translation of epidermal growth factor receptor through an unannotated terminal oligopyrimidine motif in its 5\u2019 untranslated region. We further demonstrate a physiological role of IRE1\u03b1-governed protein translation by showing that IRE1\u03b1 is essential for cardiomyocyte growth and cardiac functional maintenance under hemodynamic stress in vivo.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>These studies suggest a noncanonical, essential role of IRE1\u03b1 in orchestrating protein synthesis, which may have important implications in cardiac hypertrophy in response to pressure overload and general cell growth under other physiological and pathological conditions.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.123.067606","type":"journal-article","created":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T09:11:38Z","timestamp":1717578698000},"page":"1010-1029","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":21,"title":["IRE1\u03b1 Mediates the Hypertrophic Growth of Cardiomyocytes Through Facilitating the Formation of Initiation Complex to Promote the Translation of TOP-Motif Transcripts"],"prefix":"10.1161","volume":"150","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2060-4835","authenticated-orcid":true,"given":"Chao","family":"Li","sequence":"first","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine (C.L., G.Z., Q.L., W.S., X.W., J.A.C., X.L., H.I.M., A.F., T.G.G., J.A.H., Z.V.W.), University of Texas Southwestern Medical Center, Dallas."},{"name":"Touchstone Diabetes Center, Department of Internal Medicine (C.L., J.A.C., X.-N.S., P.E.S.), University of Texas Southwestern Medical Center, Dallas."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1663-0704","authenticated-orcid":true,"given":"Shiqian","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Finland (S.L., M.v.d.S., E.I.)."},{"name":"Minerva Foundation Institute for Medical Research, Helsinki, Finland (S.L., M.v.d.S., E.I.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8145-6701","authenticated-orcid":true,"given":"Guangyu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine (C.L., G.Z., Q.L., W.S., X.W., J.A.C., X.L., H.I.M., A.F., T.G.G., J.A.H., Z.V.W.), University of Texas Southwestern Medical Center, Dallas."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0582-2102","authenticated-orcid":true,"given":"Qinfeng","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine (C.L., G.Z., Q.L., W.S., X.W., J.A.C., X.L., H.I.M., A.F., T.G.G., J.A.H., Z.V.W.), University of Texas Southwestern Medical Center, 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