ArticleMolecular medicine reports2016
Zoledronate induces autophagic cell death in human umbilical vein endothelial cells via Beclin-1 dependent pathway activation.
Article in Molecular medicine reports, 2016. 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, 16 citations in OpenAlex.
- Advanced biomaterial-based approaches for medication-related osteonecrosis of the jaw.Open life sciences · 2026Article
- The Cellular and Mitochondrial Consequences of Mevalonate Pathway Inhibition by Nitrogen-Containing Bisphosphonates: A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Targeting endoplasmic reticulum stress-induced lymphatic dysfunction for mitigating bisphosphonate-related osteonecrosis.Clinical and translational medicine · 2024Article
- New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death.International journal of molecular sciences · 2023Review
- Could Local Application of Hypoxia Inducible Factor 1-α Enhancer Deferoxamine Be Promising for Preventing of Medication-Related Osteonecrosis of the Jaw?Biomedicines · 2023Article
- Medication-Related Osteonecrosis of the Jaws Initiated by Zoledronic Acid and Potential Pathophysiology.Dentistry journal · 2021Review
- Epidermal Growth Factor Reverses the Inhibitory Effects of the Bisphosphonate, Zoledronic Acid, on Human Oral Keratinocytes and Human Vascular Endothelial Cells In Vitro via the Epidermal Growth Factor Receptor (EGFR)/Akt/Phosphoinositide 3-Kinase (PI3K) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Pathogenesis of medication-related osteonecrosis of the jaw: a comparative study of in vivo and in vitro trials.The Journal of international medical research · 2018Review
- Beclin1 overexpression suppresses tumor cell proliferation and survival via an autophagy‑dependent pathway in human synovial sarcoma cells.Oncology reports · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zoledronate has been reported to exhibit pro‑apoptotic and anti-angiogenic effects in endothelial cells, which partially contributes to bisphosphonate‑associated osteonecrosis of the jaw (BP‑ONJ). Zoledronate can also induce autophagic cell death. The present study hypothesized that Zoledronate may activate autophagy to exert pro‑apoptotic effects in endothelial cells and aimed to investigate the effect of Zoledronate on human umbilical vein endothelial cells (HUVECs) and explore the underlying mechanisms. The current study demonstrated that Zoledronate induced autophagy in HUVECs in a dose‑dependent manner, as demonstrated by increased levels of microtubule‑associated proteins 1A/1B light chain 3B‑II (LC3B‑II) and Beclin‑1, and decreased levels of sequestome 1 (SQSTM1). In addition, treatment with chloroquine further increased LC3B‑II and increased SQSTM1 levels, indicating that Zoledronate induces autophagy by increasing autophagic activity. Flow cytometry and Hoechst 33258 staining revealed that inhibition of autophagy with 3-methyladenine markedly attenuated Zoledronate‑induced apoptosis. Furthermore, genetic knockdown of Beclin‑1 significantly inhibited autophagy and apoptosis induced by Zoledronate. The present study therefore demonstrated that Zoledronate may promote Beclin‑1‑mediated autophagy to induce endothelial cell apoptosis, and suggests that blocking autophagy may represent a novel approach for the prevention of BP‑ONJ in patients receiving Zoledronate.
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