ArticleScientific reports2018
Various roles of heme oxygenase-1 in response of bone marrow macrophages to RANKL and in the early stage of osteoclastogenesis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Heme Oxygenase-1 Differentially Controls Pigmentation in Physiological and Pathological Melanogenesis.Pigment cell & melanoma research · 2026Article
- An Alternative to Biliverdin, Mesobiliverdin IXα and Mesobiliverdin-Enriched Microalgae: A Review on the Production and Applications of Mesobiliverdin-Related Products.Molecules (Basel, Switzerland) · 2025Review
- Lysosome-Iron-Mitochondria Axis in Osteoclasts: Iron as a Central Player.Research (Washington, D.C.) · 2025Review
- Integrated single-cell and bulk RNA sequencing analysis reveal immune-related biomarkers in postmenopausal osteoporosis.Heliyon · 2024Article
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- The Therapeutic Potential of Two Egyptian Plant Extracts for Mitigating Dexamethasone-Induced Osteoporosis in Rats: Nrf2/HO-1 and RANK/RANKL/OPG Signals.Antioxidants (Basel, Switzerland) · 2024Article
- Ginsenoside compound-K attenuates OVX-induced osteoporosis via the suppression of RANKL-induced osteoclastogenesis and oxidative stress.Natural products and bioprospecting · 2023Article
- Regulating Type H Vessel Formation and Bone Metabolism via Bone-Targeting Oral Micro/Nano-Hydrogel Microspheres to Prevent Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Flavonoids fromJournal of dental sciences · 2023Article
- Kruppel-like Factors in Skeletal Physiology and Pathologies.International journal of molecular sciences · 2022Review
- Methyl 3,4-dihydroxybenzoate inhibits RANKL-induced osteoclastogenesis via Nrf2 signalingActa biochimica et biophysica Sinica · 2022Article
- Targeting Sirt1, AMPK, Nrf2, CK2, and Soluble Guanylate Cyclase with Nutraceuticals: A Practical Strategy for Preserving Bone Mass.International journal of molecular sciences · 2022Review
- Heme Oxygenase-1 Has a Greater Effect on Melanoma Stem Cell Properties Than the Expression of Melanoma-Initiating Cell Markers.International journal of molecular sciences · 2022Article
- Long Bone Mineral Loss, Bone Microstructural Changes and Oxidative Stress AfterFrontiers in physiology · 2022Article
- CYT387, a JAK-Specific Inhibitor Impedes Osteoclast Activity and Oophorectomy-Induced OsteoporosisFrontiers in pharmacology · 2022Article
- Transcription Factor KLF7 Promotes Osteoclast Differentiation by Suppressing HO-1.Frontiers in genetics · 2022Article
- HO-1 in Bone Biology: Potential Therapeutic Strategies for Osteoporosis.Frontiers in cell and developmental biology · 2021Review
- Heme Oxygenase-1 Is a Pivotal Modulator of Bone Turnover and Remodeling: Molecular Implications for Prostate Cancer Bone Metastasis.Antioxidants & redox signaling · 2020Article
- Nrf2 is required for suppressing osteoclast RANKL-induced differentiation in RAW 264.7 cells via inactivating cannabinoid receptor type 2 with AM630.Regenerative therapy · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Heme oxygenase-1 (HO-1; encoded by Hmox1), a downstream target of the Nrf2 transcription factor, has been postulated to be a negative regulator of osteoclasts (OCLs) differentiation. Here, we further explored such a hypothesis by examining HO-1 effects in different stages of osteoclastogenesis. We confirmed the inhibition of the expression of OCLs markers by Nrf2. In contrast, both the lack of the active Hmox1 gene or HO-1 silencing in OCLs precursor cells, bone marrow macrophages (BMMs), decreased their differentiation towards OCLs, as indicated by the analysis of OCLs markers such as TRAP. However, no effect of HO-1 deficiency was observed when HO-1 expression was silenced in BMMs or RAW264.7 macrophage cell line pre-stimulated with RANKL (considered as early-stage OCLs). Moreover, cobalt protoporphyrin IX (CoPPIX) or hemin, the known HO-1 inducers, inhibited OCLs markers both in RANKL-stimulated RAW264.7 cells and BMMs. Strikingly, a similar effect occurred in HO-1
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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.