ArticleAging cell2025
Targeting NAMPT-OPA1 for treatment of senile osteoporosis.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Diagnostic biomarkers for non-traumatic osteonecrosis of the femoral head : a systematic review and pathophysiological cascade network.Bone & joint research · 2026Pooled it
- P7C3 Compounds as Targeted Mitochondrial Therapeutics for Brain Disorders.CNS neuroscience & therapeutics · 2026Pooled it
- A sustained NADBioactive materials · 2026Article
- Gαi1/3 Are Essential for BMP2-Induced Osteogenesis by Bridging BMP Receptors to the Gab1 Signaling Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Natural Polysaccharide-Mediated Nano-Delivery Systems for Osteoporosis Therapy From a Gut-Bone Axis Regulatory Perspective.Advanced healthcare materials · 2026Review
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Gαi1/3 Is a Novel Regulatory Target for RANKL Signal Transduction and Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The purinergic receptor P2rx7 mediated ATP sensing is required to prevent bone aging by directing mitochondrial fitness of MSCs.Journal of advanced research · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- The association between body roundness index and osteoporosis in older patients: a cross-sectional study based on a comprehensive geriatric assessment.BMC geriatrics · 2025Article
- GPR65 Functions as a Key Factor of Bone Aging and a Novel Therapeutic Target for Osteoporosis.Aging cell · 2025Article
- Nicotinamide phosphoribosyltransferase in NADCell death discovery · 2025Review
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
- Effect of adipokines on bone marrow mesenchymal stem cell function.World journal of stem cells · 2025Review
- Targeting NAMPT-OPA1 for treatment of senile osteoporosis.Aging cell · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
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 reduced mitochondrial membrane potential, interfered with mitochondrial fusion，and increased SA protein and phenotypes. More importantly, we have confirmed that P7C3, the NAMPT activator, is a novel strategy for reducing SOP bone loss. P7C3 treatment significantly prevents BMSCs senescence by improving mitochondrial function through the NAMPT-OPA1 signaling axis. Taken together, these results reveal that NAMPT is a regulator of BMSCs senescence and osteogenic differentiation. P7C3 is a novel molecule drug to prevent the pathological progression of SOP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.