ArticleACS omega2025
Mechanisms of Ellagic Acid (EA)-Mediated Osteogenic Differentiation of Human Dental Pulp-Derived Stem Cells.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ellagic acid and bone health: a systematic review of preclinical studies on its protective role against osteoporosis.Molecular biology reports · 2026Pooled it
- Krüppel-like Factor 2 (KLF2) Regulates Autophagy, Mitophagy, Mitochondrial Health, and Function During Foam Cell Formation.Diseases & research · 2026Article
- KLF2 Promotes Ellagic Acid-Mediated Osteogenic Differentiation of Dental Pulp-Derived Stem Cells via Autophagy and Mitochondrial Regulation.Diseases & research · 2026Article
- Unraveling the Bone-Brain Communication Network.Biology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Ellagic acid (EA) is a potent antioxidant that reduces oxidative stress and promotes differentiation. By lowering the harmful levels of reactive oxygen species (ROS), EA fosters an environment conducive to the osteoblastic differentiation (OB) of stem cells. In addition, it promotes autophagy and mitophagy, which are vital for promoting differentiation. Effective autophagic activity recycles damaged organelles and proteins, meeting the energy required during differentiation and shielding from apoptosis. However, molecular mechanisms underlying the osteogenic differentiation of mesenchymal stem cells remain inadequately explored. Therefore, the current study aims to define the regulatory role of EA during the OB of dental pulp-derived stem cells (DPSC) and to study how autophagy and mitophagy are being modulated during this differentiation process. Herein, we showed that the expression level of osteoblast-specific markers, autophagy, and mitophagy-associated markers was significantly elevated during EA-mediated OB differentiation of DPSC. Moreover, we found that the EA induced the osteoblastic-specific markers through canonical BMP2 pathway molecules, reduced ROS in both basal and activated states, and induced autophagy and mitophagy molecules along with enhanced mitochondrial functions. Cell cycle analysis revealed that the G1 phase was arrested via phosphorylation of γ-H2AX, ATM, and CHK2 proteins. Furthermore, in silico analysis revealed that EA strongly binds with osteonectin, a crucial noncollagen protein involved in bone remodeling, and confirmed by Western blot analysis. These results support that EA could be a promising natural compound for bone repair and regeneration applications.
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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 OpenQuestion graph.