{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Abdellatif M"],"funding":["Austrian Science Fund FWF","Cancéropôle Ile-de-France; Fondation pour la Recherche Médicale","Association “Ruban Rose”","Institut Universitaire de France; LabEx Immuno-Oncology","Elior; Equipex Onco-Pheno-Screen; European Joint Programme on Rare Diseases","European Commission","Association pour la recherche sur le cancer","Ligue contre le Cancer (équipe labellisée); Agence National de la Recherche (ANR) – Projets blancs","Institut National du Cancer (INCa); Inserm","RHU Torino Lumière; Seerave Foundation; SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination","European Union Horizon 2020 Projects Oncobiome and Crimson","SIRIC Cancer Research and Personalized Medicine","IdEx Université de Paris","Leducq Foundation","the European Research Area Network on Cardiovascular Diseases","Fondation Carrefour; High-end Foreign Expert Program in China"],"pagination":["2500-2502"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9542397"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(10)"],"pubmed_abstract":["Although attenuated IGF1R (insulin-like growth factor 1 receptor) signaling has long been viewed to promote longevity in model organisms, adverse effects on the heart have been the subject of major concern. We observed that IGF1R is overexpressed in cardiac tissues from patients with end-stage non-ischemic heart failure, coupled to the activation of the IGF1R downstream effector AKT/protein kinase B and inhibition of ULK1 (unc-51 like autophagy activating kinase 1). Transgenic overexpression of human IGF1R in cardiomyocytes from mice initially induces physiological cardiac hypertrophy and superior function, but later in life confers a negative impact on cardiac health, causing macroautophagy/autophagy inhibition as well as impaired oxidative phosphorylation, thus reducing life expectancy. "],"journal":["Autophagy"],"pubmed_title":["Spermidine overrides INSR (insulin receptor)-IGF1R (insulin-like growth factor 1 receptor)-mediated inhibition of autophagy in the aging heart."],"pmcid":["PMC9542397"],"funding_grant_id":["US23/CNRS UMS3655","through grant I3301-MINOTAUR","GDW20171100085","ANR-18-IDEX-000"],"pubmed_authors":["Sedej S","Madeo F","Kroemer G","Abdellatif M"],"additional_accession":[]},"is_claimable":false,"name":"Spermidine overrides INSR (insulin receptor)-IGF1R (insulin-like growth factor 1 receptor)-mediated inhibition of autophagy in the aging heart.","description":"Although attenuated IGF1R (insulin-like growth factor 1 receptor) signaling has long been viewed to promote longevity in model organisms, adverse effects on the heart have been the subject of major concern. We observed that IGF1R is overexpressed in cardiac tissues from patients with end-stage non-ischemic heart failure, coupled to the activation of the IGF1R downstream effector AKT/protein kinase B and inhibition of ULK1 (unc-51 like autophagy activating kinase 1). Transgenic overexpression of human IGF1R in cardiomyocytes from mice initially induces physiological cardiac hypertrophy and superior function, but later in life confers a negative impact on cardiac health, causing macroautophagy/autophagy inhibition as well as impaired oxidative phosphorylation, thus reducing life expectancy. ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-18T21:01:35.529Z","creation":"2025-04-07T09:02:33.68Z"},"accession":"S-EPMC9542397","cross_references":{"pubmed":["35786404"],"doi":["10.1080/15548627.2022.2095835"]}}