ReviewBoneKEy reports2015
Focus on the p38 MAPK signaling pathway in bone development and maintenance.
Review in BoneKEy reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Effects of Caffeic Acid and Its Derivatives on Bone: A Systematic Review.Drug design, development and therapy · 2021Pooled it
- Targeting cellular senescence mitigates chemotherapy-induced bone loss in young and aged mice.GeroScience · 2026Article
- Bta-miR-146a Inhibits Proliferation and Promotes Apoptosis of Bovine Immature Sertoli Cells by Targeting SMAD4 via the TGF-β/MAPK Signaling Pathway.International journal of molecular sciences · 2026Article
- MSC-Derived Apoptotic Vesicles Restore Bone Marrow Niche Homeostasis in Postmenopausal Osteoporosis by miRNA-Mediated Suppression of MAPK and NF-κB Signaling Nodes.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Non-covalent proteasome inhibitor PI1840 suppresses osteoclastogenesis and prevents LPS-induced osteolysis in mice.Inflammopharmacology · 2026Article
- Translational Nanomedicine for Osteoporosis: Bridging Bone Signaling Networks and Targeted Delivery Systems.International journal of nanomedicine · 2026Review
- Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer.Cancer cell international · 2025Review
- Multi-Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures.Journal of neurochemistry · 2025Article
- Selective Modulation of Osteoclast Function byToxins · 2025Article
- Landscape analysis of m6A modification reveals the dysfunction of bone metabolism in osteoporosis mice.Heliyon · 2025Article
- Phospholipase C β4 promotes RANKL-dependent osteoclastogenesis by interacting with MKK3 and p38 MAPK.Experimental & molecular medicine · 2025Article
- Mixtures of PRR Ligands Partly Mimic the Immunomodulatory Response ofStem cells international · 2025Article
- During high salt treatment myeloid p38α/MAPK fosters osteoclast activity and inflammatory macrophage responses promoting orthodontic tooth movement.Frontiers in immunology · 2025Article
- MicroRNA functions in osteogenic differentiation of periodontal ligament stem cells: a scoping review.Frontiers in oral health · 2025Review
- Effects of different temperatures on chondrocyte growth: a transcriptomic analysis.BMC medical genomics · 2024Article
- Irisin as an agent for protecting against osteoporosis: A review of the current mechanisms and pathways.Journal of advanced research · 2024Review
- Involvement of RAMP1/p38MAPK signaling pathway in osteoblast differentiation in response to mechanical stimulation: a preliminary study.Journal of orthopaedic surgery and research · 2024Article
- Therapeutic potential of a prominent dihydroxyflavanone pinocembrin for osteolytic bone disease:Journal of orthopaedic translation · 2024Article
- Magnesium-containing bioceramics stimulate exosomal miR-196a-5p secretion to promote senescent osteogenesis through targetingBioactive materials · 2024Article
- Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p38 mitogen-activated protein kinase (MAPK) signaling pathway can be activated in response to a wide range of extracellular signals. As a consequence, it can generate many different biological effects that depend on the stimulus and on the activated cell type. Therefore, this pathway has been found to regulate many aspects of tissue development and homeostasis. Recent work with the aid of genetically modified mice has highlighted the physiological functions of this pathway in skeletogenesis and postnatal bone maintenance. In this review, emphasis is given to the roles of the p38 MAPK pathway in chondrocyte, osteoblast and osteoclast biology. In particular, we describe the molecular mechanisms of p38 MAPK activation and downstream targets. The requirement of this pathway in physiological bone development and homeostasis is demonstrated by the ability of p38 MAPK to regulate master transcription factors controlling geneses and functions of chondrocytes, osteoblasts and osteoclasts.
Identifiers
What OpenQuestion holds
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.