ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Osmolarity-Induced Altered Intracellular Molecular Crowding Drives Osteoarthritis Pathology.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Nanozyme-Integrated Hydrogel Targeting AGEs for Diabetic Osteoarthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- How does cytoplasmic crowding affect reaction rates?Molecular cell · 2026Review
- Machine learning predicts clinical response to platelet-rich plasma therapy in knee osteoarthritis.Frontiers in medicine · 2026Article
- A Multidimensional Definition of Pre-Osteoarthritis: Toward 21st-Century Subclinical Detection and Targeted Intervention.International journal of molecular sciences · 2025Review
- Article
- Underestimated role of macromolecular crowding in bioengineeredMaterials today. Bio · 2025Article
- Cell-imprinted substrates as biomimetic platforms for osteoarthritis modeling with mesenchymal stem cells.BioImpacts : BI · 2025Article
- Dissecting SOX9 dynamics reveals its differential regulation in osteoarthritis.Journal of cellular physiology · 2024Article
- Article
- Osmolarity-Induced Altered Intracellular Molecular Crowding Drives Osteoarthritis Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA) is a multifactorial degenerative joint disease of which the underlying mechanisms are yet to be fully understood. At the molecular level, multiple factors including altered signaling pathways, epigenetics, metabolic imbalance, extracellular matrix degradation, production of matrix metalloproteinases, and inflammatory cytokines, are known to play a detrimental role in OA. However, these factors do not initiate OA, but are mediators or consequences of the disease, while many other factors causing the etiology of OA are still unknown. Here, it is revealed that microenvironmental osmolarity can induce and reverse osteoarthritis-related behavior of chondrocytes via altered intracellular molecular crowding, which represents a previously unknown mechanism underlying OA pathophysiology. Decreased intracellular crowding is associated with increased sensitivity to proinflammatory triggers and decreased responsiveness to anabolic stimuli. OA-induced lowered intracellular molecular crowding could be renormalized via exposure to higher extracellular osmolarity such as those found in healthy joints, which reverse OA chondrocyte's sensitivity to catabolic stimuli as well as its glycolytic metabolism.
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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.