ReviewMedComm2025
Posttranslational Modification in Bone Homeostasis and Osteoporosis.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed.
- Mechanical Unloading Inhibits Osteoblast Differentiation via Downregulation of OGT-Mediated O-GlcNAcylation.Current issues in molecular biology · 2026Article
- Research Progress on Mechanisms of Milk-Derived Functional Components in Regulating Bone Health and the Gut-Bone Axis.Nutrients · 2026Review
- Biomolecular condensates as dynamic regulators of musculoskeletal homeostasis, disease, and therapeutic challenges.Bone research · 2026Review
- Hydrogels: current biomedical applications and future directions.Molecular biomedicine · 2026Review
- ZDHHC8-mediated S-palmitoylation of RAD21 causes mitochondrial dysfunction in diabetic nephropathy via inhibiting ACSM3 transcription.Cell death and differentiation · 2026Article
- Article
- Lactylation Reprogramming in the Bone Infection Microenvironment Identifies PGK1 K361 as a Potential Therapeutic Target for Osteogenic Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting post-translational modifications: novel insights into bone metabolic diseases.Journal of advanced research · 2026Review
- USP8-mediated mitochondrial regulation in osteoclasts is essential for skeletal development.Cellular and molecular life sciences : CMLS · 2026Article
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
- Dabigatran Attenuates Osteoporosis by Balancing Osteoblastogenesis and Osteoclastogenesis by Targeting PRKAB1 and RELA.Research (Washington, D.C.) · 2026Article
- Decoding Epigenetic Switches: How Histone Acetylation/Deacetylation Regulates Mononuclear/Macrophage Fate in Bone Disorders.International journal of biological sciences · 2026Review
- miR-202-5p mitigates the advancement of osteoporosis through the regulation of PTEN.Journal of orthopaedic surgery and research · 2025Article
- Development and validation of an interpretable machine learning model for osteoporosis prediction using routine blood tests: a retrospective cohort study.BMC medical informatics and decision making · 2025Article
- Epigenetic Dysregulation and Osteocyte Senescence: Convergent Drivers of Osteosarcopenia in Aging Bone and Muscle.Aging and disease · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone is responsible for providing mechanical protection, attachment sites for muscles, hematopoiesis micssroenvironment, and maintaining balance between calcium and phosphorate. As a highly active and dynamically regulated organ, the balance between formation and resorption of bone is crucial in bone development, damaged bone repair, and mineral homeostasis, while dysregulation in bone remodeling impairs bone structure and strength, leading to deficiency in bone function and skeletal disorder, such as osteoporosis. Osteoporosis refers to compromised bone mass and higher susceptibility of fracture, resulting from several risk factors deteriorating the balanced system between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. This balanced system is strictly regulated by translational modification, such as phosphorylation, methylation, acetylation, ubiquitination, sumoylation, glycosylation, ADP-ribosylation, S-palmitoylation, citrullination, and so on. This review specifically describes the updating researches concerning bone formation and bone resorption mediated by posttranslational modification. We highlight dysregulated posttranslational modification in osteoblast and osteoclast differentiation. We also emphasize involvement of posttranslational modification in osteoporosis development, so as to elucidate the underlying molecular basis of osteoporosis. Then, we point out translational potential of PTMs as therapeutic targets. This review will deepen our understanding between posttranslational modification and osteoporosis, and identify novel targets for clinical treatment and identify future directions.
Indexed as
Identifiers
What Socratic 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 Socratic graph.