ArticleCell death discovery2022
MiR-148a deletion protects from bone loss in physiological and estrogen-deficient mice by targeting NRP1.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- The characteristic expression of circulatingFrontiers in endocrinology · 2024Pooled it
- Feedback loops between DNMT1 and autophagy as well as senescence promotes organ aging and canities.Autophagy · 2026Article
- Neuropilin‑1: Emerging roles in nerve‑vessel‑bone coupling during fracture repair (Review).International journal of molecular medicine · 2026Review
- Acupuncture-Mediated Neuro-Immune Regulation in Musculoskeletal Pain: Mechanisms and Therapeutic Perspectives.Journal of pain research · 2026Review
- Functional Analysis of miR-148a: A Differentially Expressed microRNA in Hemifacial Microsomia.Current molecular medicine · 2026Article
- Review
- miR-34c-5p targets Notch2 to promote fracture healing.Journal of orthopaedic surgery and research · 2025Article
- A microsphere loaded with chondrocyte-targeting exosomes continuously deliver miR-148a for osteoarthritis therapy.Materials today. Bio · 2025Article
- Mettl7a alleviated bone loss in osteoporosis mice by targeting the O-GlcNAcylation of Bsp via m6A methylation.Stem cells translational medicine · 2025Article
- Dysregulation of miR-106a-5p/PTEN axis associated with progression and diagnostic of postmenopausal osteoporosis.Journal of orthopaedic surgery and research · 2025Article
- Non-coding RNAs in osteoarthritis and osteoporosis-related hip fractures: molecular biomarkers for precision diagnosis and prognosis.Frontiers in endocrinology · 2025Review
- MicroRNAs and their Modulatory Effect on the Hallmarks of Osteosarcopenia.Current osteoporosis reports · 2024Review
- Noncoding RNAs in skeletal development and disorders.Biological research · 2024Review
- Review
- Decoding the secrets of longevity: unraveling nutraceutical and miRNA-Mediated aging pathways and therapeutic strategies.Frontiers in aging · 2024Review
- Circ_KIAA0922 regulates Saos-2 cell proliferation and osteogenic differentiation by regulating the miR-148a-3p/SMAD5 axis and activating the TGF-β signaling pathway.Intractable & rare diseases research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone metabolic homeostasis is largely dependent on the dynamic balance between osteoblasts and osteoclasts. MicroRNAs (miRNAs) play critical roles in regulating bone metabolism. In this study, we explored the role of a new miRNA (miR-148a) in osteoporosis. We compared the bone phenotype between miR-148a knockout (KO) mice and the wild-type (WT) littermates. We found miR-148a KO mice exhibited an increased bone mass phenotype and decreased osteoclastogenesis compared to the WT group. In vitro, miR-148a overexpression promoted osteoclastogenesis and bone resorption function. Mechanistically, NRP1 was identified as a novel direct target of miR-148a, and NRP1 silencing reversed the effect of miR-148a knockout. In OVX and calvarial osteolysis models, miR-148a KO protects mice against excessive bone resorption, while miR-148a agomiR/AAV-shNRP1 accelerates pathologic bone loss. Finally, the miR-148a level was found to be positively correlated with β-CTX in postmenopausal osteoporosis (PMOP) serum specimens. In summary, our findings revealed that miR-148a genetic deletion ameliorates bone loss under physiological and pathological conditions by targeting NRP1. In osteoclast-related bone metabolic diseases such as PMOP, miR-148a may be an attractive therapeutic target in the future.
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.