{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T11:09:50Z","timestamp":1784113790207,"version":"3.55.0"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,2,3]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Heart failure is a major cause of global morbidity and mortality, often complicated by ventricular arrhythmias (VAs) that worsen prognosis. The\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      (signal recognition particle receptor beta subunit) is an endoplasmic reticulum membrane\u2010anchored protein involved in protein processing.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Male C57BL\/6 mice received tail vein injections of adeno\u2010associated virus to cardiac\u2010specifically overexpress or knock down\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      . A pressure overload\u2010induced heart failure model was established via aortic banding 3\u2009weeks later. Cardiac function, structural\/electrical remodeling, and VA susceptibility were evaluated 4\u2009weeks post aortic banding using echocardiography, ECG, in\u00a0vivo electrophysiology, and molecular\/pathological analyses. In\u00a0vitro, primary neonatal mouse cardiomyocytes and fibroblasts were transfected with\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      \u2010modulating adenoviruses to investigate its role in hypertrophy and fibrosis. Pathway inhibitors were used to confirm mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      knockdown improved pressure overload\u2010induced cardiac structural and electrical remodeling, reducing VAs. Conversely,\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      overexpression exacerbated these abnormalities and increased VA incidence. In\u00a0vitro,\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      knockdown alleviated angiotensin II\u2010induced cardiomyocyte hypertrophy and TGF\u2010\u03b2 (transforming growth factor\u2010\u03b2)\u2010induced fibroblast fibrosis, whereas its overexpression aggravated them. Mechanistically,\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      promoted VA vulnerability by activating endoplasmic reticulum stress and the TLR4\/CaMKII\/NF\u2010\u03baB (Toll\u2010like receptor 4\/Ca2+\/calmodulin\u2010dependent protein kinase II\/nuclear factor kappa B) signaling pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      <jats:italic toggle=\"yes\">Srprb<\/jats:italic>\n                      knockdown improved ventricular remodeling and suppressed VAs in mice with heart failure, whereas its overexpression has opposite effects. These actions were mediated through regulation of endoplasmic reticulum stress and the TLR4\/CaMKII\/NF\u2010\u03baB pathway.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.044103","type":"journal-article","created":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T10:20:27Z","timestamp":1769077227000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Signal Recognition Granule Receptor Beta Subunit Promotes Arrhythmogenic Remodeling in the Heart Failure Mice"],"prefix":"10.1161","volume":"15","author":[{"given":"Jingjing","family":"Zhang","sequence":"first","affiliation":[{"name":"Renmin Hospital of Wuhan University","place":["Wuhan, People\u2019s Republic of China"]},{"name":"Cardiovascular Research Institute of Wuhan University","place":["Wuhan, People\u2019s Republic of China"]},{"name":"Hubei Key Laboratory of Cardiology","place":["Wuhan, People\u2019s Republic of 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