ReviewJournal of inflammation research2023
The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis.
Review in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- From mechanisms to therapeutics: a narrative review on pyroptosis and autophagy in osteoporosis.Annals of medicine · 2025Pooled it
- Blockade of NLRP3 alleviates systemic lupus erythematosus-induced osteoporosis through dual modulation of osteogenesis and osteoclastogenesis.Bone reports · 2026Article
- Article
- An Inulin-Type Atractylodes Macrocephala Polysaccharide Alleviates Weightlessness-Induced Bone Loss in Association with the Nrf2/HO-1 Pathway.Nutrients · 2026Article
- DDX39B drives the m6A modification of LDHA to promote trophoblast proliferation.Molecular genetics and genomics : MGG · 2026Article
- Food and Medicine Homologous Plants in Osteoporosis: A Scoping Review of Preclinical Evidence.Food science & nutrition · 2026Review
- The functional roles and mechanisms of polyamines in age-related bone diseases.Cellular and molecular life sciences : CMLS · 2025Review
- Osteoporosis: molecular pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The maintenance of bone homeostasis is dynamically regulated by osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Abnormal differentiation of osteoclast and insufficient osteoblast production can cause bone diseases such as osteoporosis. As one of the highly conserved catabolic pathways in eukaryotic cells, autophagy plays an important role in maintaining cell homeostasis, stress injury repair, proliferation and differentiation. Numerous studies have found that autophagy activity is essential for the survival, differentiation and function of bone cells, and that regulation of autophagy can affect the metabolism of osteoblasts and osteoclasts, thus affecting bone homeostasis. Therefore, using autophagy as a theme, this review outlines the basic process of autophagy, the relationship between autophagy and osteoblasts and osteoclasts, and summarizes the latest research progress of common autophagic signaling pathways in osteoblasts and osteoclasts. The regulatory effects of protein molecules and natural compounds on the autophagy pathway of osteoblasts and osteoclasts discovered in current research are summarized and discussed. This will help to further clarify the mechanism of osteoporosis, understand the relationship between autophagy and osteoporosis, and propose new therapeutic strategies and new ideas for anti-osteoporosis.
Indexed as
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.