ReviewCurrent osteoporosis reports2011
Events in articular chondrocytes with aging.
Review in Current osteoporosis reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- Cabozantinib prevents AGEs-induced degradation of type 2 collagen and aggrecan in human chondrocytes.Aging · 2023Article
- Osteoarthritis: Role of Peroxisome Proliferator-Activated Receptors.International journal of molecular sciences · 2023Review
- How are Aging and Osteoarthritis Related?Aging and disease · 2023Review
- Relationship between Outerbridge Scale and Chondropathy Femorotibial Joint in Relation to Gender and Age-The Use of 1.5T and 3.0T MRI Scanners.Medicina (Kaunas, Lithuania) · 2022Observational
- Regenerative Engineering Animal Models for Knee Osteoarthritis.Regenerative engineering and translational medicine · 2022Article
- The role of AGEs in pathogenesis of cartilage destruction in osteoarthritis.Bone & joint research · 2022Article
- Cardamonin Inhibited IL-1β Induced Injury by Inhibition of NLRP3 Inflammasome via Activating Nrf2/NQO-1 Signaling Pathway in Chondrocyte.Journal of microbiology and biotechnology · 2021Article
- Common Musculoskeletal Disorders in the Elderly: The Star Triad.Journal of clinical medicine · 2020Review
- miR-195 contributes to human osteoarthritis via targeting PTHrP.Journal of bone and mineral metabolism · 2019Article
- Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes.BioMed research international · 2017Article
- Ageing in the musculoskeletal system.Acta orthopaedica · 2016Review
- Context-specific protection of TGFα null mice from osteoarthritis.Scientific reports · 2016Article
- Oxidative changes and signalling pathways are pivotal in initiating age-related changes in articular cartilage.Annals of the rheumatic diseases · 2016Article
- Cytokine profiles in the joint depend on pathology, but are different between synovial fluid, cartilage tissue and cultured chondrocytes.Arthritis research & therapy · 2014Article
- Linked decreases in liver kinase B1 and AMP-activated protein kinase activity modulate matrix catabolic responses to biomechanical injury in chondrocytes.Arthritis research & therapy · 2013Article
- The age-related changes in cartilage and osteoarthritis.BioMed research international · 2013Review
- Effect of age and cytoskeletal elements on the indentation-dependent mechanical properties of chondrocytes.PloS one · 2013Article
- Increased type II collagen cleavage by cathepsin K and collagenase activities with aging and osteoarthritis in human articular cartilage.Arthritis research & therapy · 2012Article
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
Abstract
It is well accepted that aging is one of the most prominent risk factors for the initiation and progression of osteoarthritis. One of the most pronounced age-related changes in chondrocytes is the exhibition of a senescent phenotype, which is the result of several factors including the accumulation of reactive oxygen species and advanced glycation end products. Compared with a normal chondrocyte, senescent chondrocytes exhibit an impaired ability to respond to many mechanical and inflammatory insults to the articular cartilage. Furthermore, protein secretion is altered in aging chondrocytes, demonstrated by a decrease in anabolic activity and increased production of proinflammatory cytokines and matrix-degrading enzymes. Together, these events may make the articular cartilage matrix more susceptible to damage and lead to the onset of osteoarthritis. A better understanding of the mechanisms underlying age-related chondrocyte pathophysiology may be critical for the development of novel therapeutic interventions for progressive joint diseases.
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.