ReviewBiomedicines2024
Cellular Senescence: The Driving Force of Musculoskeletal Diseases.
Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses 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
22 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Evidence gaps in the effects of exercise on SASP-Related biomarkers in older adults: a systematic review and meta-analysis of randomized controlled trials.BMC geriatrics · 2026Pooled it
- Bone physiological adaptations to whole-body vibration in mouse models: A Systematic Review.PloS one · 2026Pooled it
- Review
- Article
- Association between uric acid to high-density lipoprotein cholesterol ratio (UHR) and osteoporosis in type 2 diabetes with MASLD.Asia Pacific journal of clinical nutrition · 2026Article
- Microbiota-derived indole-3-propionic acid extends lifespan in Drosophila and improves muscle and bone health in mice.GeroScience · 2026Article
- Immune cell senescence and chronic bone diseases: osteoimmune mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Myofascial pain in older adults: a geroscience-informed framework integrating precision geriatrics and digital therapeutics.Frontiers in aging neuroscience · 2026Review
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- Targeting subchondral osteoporosis in osteoarthritis: biomechanical crosstalk and the therapeutic rationale for inflammatory microenvironment remodeling.Frontiers in immunology · 2026Review
- Cellular senescence in age-related musculoskeletal diseases: intercellular communication as a driver of disease pathogenesis.Frontiers of medicine · 2025Article
- Modulation of cellular senescence in psoriatic arthritis: exploring the potential impact of bDMARDs on telomere length, mtDNA copy number, and oxidative damage.Clinical and experimental medicine · 2025Article
- Klotho Deficiency Promotes Skeletal Muscle Weakness and Is Associated with Impaired Motor Unit Connectivity.International journal of molecular sciences · 2025Article
- Which Approach to Choose to Counteract Musculoskeletal Aging? A Comprehensive Review on the Multiple Effects of Exercise.International journal of molecular sciences · 2025Review
- Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases.Biomedicines · 2025Review
- Klotho deficiency promotes skeletal muscle weakness and is associated with impaired motor unit connectivity.bioRxiv : the preprint server for biology · 2025Article
- Article
- AMP-activated protein kinase (AMPK) is essential for tendon homeostasis and prevents premature senescence and ectopic calcification.bioRxiv : the preprint server for biology · 2025Article
- Bone Adaptations to a Whole Body Vibration Protocol in Murine Models of Different Ages: A Preliminary Study on Structural Changes and Biomarker Evaluation.Journal of functional morphology and kinesiology · 2025Article
- SIRT1 and exercise-induced bone metabolism: a regulatory nexus.Frontiers in cell and developmental biology · 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aging of the world population is closely associated with an increased prevalence of musculoskeletal disorders, such as osteoporosis, sarcopenia, and osteoarthritis, due to common genetic, endocrine, and mechanical risk factors. These conditions are characterized by degeneration of bone, muscle, and cartilage tissue, resulting in an increased risk of fractures and reduced mobility. Importantly, a crucial role in the pathophysiology of these diseases has been proposed for cellular senescence, a state of irreversible cell cycle arrest induced by factors such as DNA damage, telomere shortening, and mitochondrial dysfunction. In addition, senescent cells secrete pro-inflammatory molecules, called senescence-associated secretory phenotype (SASP), which can alter tissue homeostasis and promote disease progression. Undoubtedly, targeting senescent cells and their secretory profiles could promote the development of integrated strategies, including regular exercise and a balanced diet or the use of senolytics and senomorphs, to improve the quality of life of the aging population. Therefore, our review aimed to highlight the role of cellular senescence in age-related musculoskeletal diseases, summarizing the main underlying mechanisms and potential anti-senescence strategies for the treatment of osteoporosis, sarcopenia, and osteoarthritis.
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.