ArticleHuman cell2022
STK11 overexpression prevents glucocorticoid-induced osteoporosis via activating the AMPK/SIRT1/PGC1α axis.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Mitochondrial homeostasis in bone aging: Unraveling dysfunctional pathways and developing precision therapies.Fundamental research · 2026Review
- Molecular Mechanisms and Therapeutic Targets for Pain Following Osteoporotic Vertebral Fractures.Journal of pain research · 2026Review
- Review
- Sirt1: An Increasingly Interesting Molecule with a Potential Role in Bone Metabolism and Osteoporosis.Biomolecules · 2024Review
- Machine learning-mediated identification of ferroptosis-related genes in osteonecrosis of the femoral head.FEBS open bio · 2024Article
- Traditional Chinese medicine in osteoporosis: from pathogenesis to potential activity.Frontiers in pharmacology · 2024Review
- Zoledronate Promotes Peri-Implant Osteogenesis in Diabetic Osteoporosis by the AMPK Pathway.Calcified tissue international · 2023Article
- Why Is Iron Deficiency/Anemia Linked to Alzheimer's Disease and Its Comorbidities, and How Is It Prevented?Biomedicines · 2023Review
- Effect of 11-Deoxycorticosterone in the Transcriptomic Response to Stress in Rainbow Trout Skeletal Muscle.Genes · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis (OP) is a frequent orthopedic disease characterized by pain, fractures and deformities. Glucocorticoids are the most common cause of secondary osteoporosis. Here, we aim to explore the function and mechanism of STK11 in glucocorticoid (GC)-induced OP. Human mesenchymal stromal cells (hMSCs) were differentiated under osteogenic or adipogenic culture medium. An in-vitro OP model was induced by dexamethasone (DEX). The viability, differentiation, apoptosis, and ROS level were evaluated for investigating the functions of SKT11 on hMSCs. The SIRT1 inhibitor EX-527, PGC1α inhibitor SR-18292, and AMPK activator metformin were administered into hMSCs for confirming the mechanism of SKT11. Our results showed that STK11 was down-regulated in OP tissues, as well as DEX-treated hMSCs. Overexpressing STK11 attenuated DEX-mediated inhibition of osteogenic differentiation and heightened the activation of the AMPK/SIRT1/PGC1α pathway, whereas STK11 knockdown exerted opposite effects. Inhibiting SIRT1 or PGC1α repressed the promotive effect of STK11 on osteogenic differentiation of hMSCs, while activation of AMPK abated the inhibitory effect of STK11 knockdown on osteogenic differentiation of hMSCs. In conclusion, this study revealed that overexpressing STK11 dampened GC-induced OP by activating the AMPK/SIRT1/PGC1α axis.
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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 OpenQuestion graph.