{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bai CW"],"funding":["Nuclear Medicine Technology Innovation Project by China Nuclear Medical","Social Development Key Programs of Jiangsu Province-Advanced Clinical Technology","Jiangsu Provincial Medical Key Discipline (Laboratory) Cultivation Unit","Youth Excellence Talent Program of the Second Affiliated Hospital of Soochow University","Gusu health talent plan-research project","Scientific research project of Jiangsu Provincial Health Commission","National Natural Science Foundation of China","Clinical Innovation and Interdisciplinary Translation Project of Suzhou Medical College, Soochow University","Gusu health talent plan-special talents C","China National Nuclear Corporation Young talent project","Natural Science Foundation of Jiangsu Province"],"pagination":["e14400"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11896342"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(3)"],"pubmed_abstract":["Senescence of bone marrow mesenchymal stem cells (BMSCs) impairs their stemness and osteogenic differentiation, which is the principal cause of senile osteoporosis (SOP). Imbalances in nicotinamide phosphoribosyltransferase (NAMPT) homeostasis have been linked to aging and various diseases. Herein, reduction of NAMPT and impaired osteogenesis were observed in BMSCs from aged human and mouse. Knockdown of Nampt in BMSCs promotes lipogenic differentiation and increases age-related bone loss. Overexpression of Nampt ameliorates the senescence-associated (SA) phenotypes in BMSCs derived from aged mice, as well as promoting osteogenic potential. Mechanistically, NAMPT inhibits BMSCs senescence by facilitating OPA1 expression, which is essential for mitochondrial dynamics. The defect of NAMPT re"],"journal":["Aging cell"],"pubmed_title":["Targeting NAMPT-OPA1 for treatment of senile osteoporosis."],"pmcid":["PMC11896342"],"funding_grant_id":["(2021) 021, (2022) 009","ZHYLTD2023001","BE2023705","Z2022010","ML12301523","XKTJ-RC202406","82172425, 82472515, 82102611, 82402826","BK20210089","JSDW202223","GSWS2021015, GSWS2022038"],"pubmed_authors":["Yang X","Qin Q","Bai JY","Zhou XZ","Shan HJ","Tian B","Gao X","Bai CW","Shi X","Zhang MC"],"additional_accession":[]},"is_claimable":false,"name":"Targeting NAMPT-OPA1 for treatment of senile osteoporosis.","description":"Senescence of bone marrow mesenchymal stem cells (BMSCs) impairs their stemness and osteogenic differentiation, which is the principal cause of senile osteoporosis (SOP). Imbalances in nicotinamide phosphoribosyltransferase (NAMPT) homeostasis have been linked to aging and various diseases. Herein, reduction of NAMPT and impaired osteogenesis were observed in BMSCs from aged human and mouse. Knockdown of Nampt in BMSCs promotes lipogenic differentiation and increases age-related bone loss. Overexpression of Nampt ameliorates the senescence-associated (SA) phenotypes in BMSCs derived from aged mice, as well as promoting osteogenic potential. Mechanistically, NAMPT inhibits BMSCs senescence by facilitating OPA1 expression, which is essential for mitochondrial dynamics. The defect of NAMPT re","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-03T04:43:18.347Z","creation":"2025-04-06T22:14:10.583Z"},"accession":"S-EPMC11896342","cross_references":{"pubmed":["39543818"],"doi":["10.1111/acel.14400"]}}