ArticleMolecular medicine reports2022
Omentin‑1 induces osteoblast viability and differentiation via the TGF‑β/Smad signaling pathway in osteoporosis.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Lipid Metabolic Reprogramming in Periodontitis-Associated Alveolar Bone Remodeling: Mechanisms, Signaling Pathways, and Therapeutic Implications.Biomolecules · 2026Review
- The role of omentin-1 in female reproduction: a critical review.The Journal of reproduction and development · 2026Review
- Upregulation of lncRNA SSTR5-AS1 promotes osteoblast differentiation and reduces apoptosis.Journal of orthopaedic surgery and research · 2025Article
- Exploration of the potential mechanism of cyclolinopeptides-mediated antiosteoporosis effects via network pharmacology analysis.BMC complementary medicine and therapies · 2025Article
- Understanding the Role of Adipokines in Cardiometabolic Dysfunction: A Review of Current Knowledge.Biomolecules · 2025Review
- Omentin-General Overview of Its Role in Obesity, Metabolic Syndrome and Other Diseases; Problem of Current Research State.Biomedicines · 2025Review
- Probiotic biofilm modified scaffolds for facilitating osteomyelitis treatment through sustained release of bacteriophage and regulated macrophage polarization.Materials today. Bio · 2025Article
- Identification of Cystatin 3 as a Potential Diagnostic Biomarker for Osteoporosis Using Machine Learning.Journal of inflammation research · 2025Article
- p-Smad3 differentially regulates the cytological behavior of osteoclasts before and after osteoblasts maturation.Molecular biology reports · 2024Article
- Adipokines regulate mesenchymal stem cell osteogenic differentiation.World journal of stem cells · 2023Review
- Novel Adipokines and Their Role in Bone Metabolism: A Narrative Review.Biomedicines · 2023Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is a bone‑related disease that results from impaired bone formation and excessive bone resorption. The potential value of adipokines has been investigated previously, due to their influence on osteogenesis. However, the osteogenic effects induced by omentin‑1 remain unclear. The aim of the present study was to determine the regulatory effects of omentin‑1 on osteoblast viability and differentiation, as well as to explore the underlying molecular mechanism. The present study investigated the effects of omentin‑1 on the viability and differentiation of mouse pre‑osteoblast cells (MC3T3‑E1) using quantitative and qualitative measures. A Cell Counting Kit‑8 assay was used to assess the viability of MC3T3‑E1 cells following treatment with different doses of omentin‑1. Omentin‑1 and bone morphogenetic protein (BMP) inhibitor were added to osteogenic induction mediums in different ways to assess their effect. The alkaline phosphatase (ALP) activity and Alizarin Red S (ARS) staining of MC3T3‑E1 cells treated with omentin‑1 and/or BMP inhibitor were used to examine the effects of omentin‑1 on differentiation and mineralization. Western blotting was used to further explore its potential mechanism, and to study the role of omentin‑1 on the viability and differentiation of osteoblasts. The results showed that omentin‑1 altered the viability of MC3T3‑E1 cells in a dose‑dependent manner. Omentin‑1 treatment significantly increased the expression of members of the TGF‑β/Smad signaling pathway. In the omentin‑1 group, the ALP activity of the MC3T3‑E1 cells was increased, and the ARS staining area was also increased. The mRNA and protein expression levels of BMP2, Runt‑related transcription factor 2, collagen1, osteopontin, osteocalcin and osterix in the omentin‑1 group were also significantly upregulated. All these effects were reversed following treatment with SIS3 HCl. These results demonstrated that omentin‑1 can significantly promote osteoblast viability and differentiation via the TGF‑β/Smad signaling pathway, thereby promoting bone formation and preventing osteoporosis.
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