ArticleArthritis & rheumatology (Hoboken, N.J.)2025
Regulation of Chondrocyte Metabolism and Osteoarthritis Development by Sirt5 Through Protein Lysine Malonylation.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- Critical role of Sirtuin 6 (SIRT6) in osteoarthritis chondrocytes: the interaction among various biological processes.Annals of medicine · 2026Review
- Identification and Validation of a Novel WNK2 Inhibitor: A New Genetically Informed Target for Osteoarthritis Drug Development.ACS omega · 2026Article
- The SIRT5-SUCLG2 desuccinylation axis delays ovarian aging via a mitochondrial-epigenetic regulatory mechanism.Nature communications · 2026Article
- Enolase 2-mediated lactylation-dependent disruption of the GNL3-MDM2-p53 axis in age-related osteoarthritis.Cellular & molecular biology letters · 2026Article
- PIEZO1 variants that reduce open channel probability are associated with familial osteoarthritis.The Journal of biological chemistry · 2026Article
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- Lineage plasticity and signal dysregulation define the cellular trajectory of osteoarthritis progression.Clinical and experimental medicine · 2025Article
- Lysine malonylation as a therapeutic target: implications for metabolic, inflammatory, and oncological disorders.Amino acids · 2025Review
- Assessment of Knee Hyperalgesia in Mice using Pressure Application Measurement.Journal of visualized experiments : JoVE · 2025Article
Corrections and comments
- Update of
Authors and funding
12 authors.
Funding
Abstract
objectiveChondrocytemetabolic dysfunction plays an important role in osteoarthritis (OA) development during aging and obesity. Protein posttranslational modifications (PTMs) have recently emerged as an important regulator of cellular metabolism. We aim to study one type of PTM, lysine malonylation (MaK), and its regulator sirtuin 5 (Sirt5) in OA development.
methodsHuman and mouse cartilage tissues were used to measure SIRT5 and MaK levels. Both systemic and cartilage-specific conditional knockout mouse models were subject to high-fat diet treatment to induce obesity and OA. Proteomics analysis was performed in Sirt5
resultsWe found that SIRT5 decreases while MaK increases in the cartilage during aging. A combination of Sirt5 deficiency and obesity exacerbates joint degeneration in a sex-dependent manner in mice. We further delineate the malonylome in chondrocytes, pinpointing MaK's predominant impact on various metabolic pathways, such as carbon metabolism and glycolysis. Lastly, we identified a rare coding mutation in SIRT5 that dominantly segregates in a family with OA. The mutation results in substitution of an evolutionally invariant phenylalanine to leucine (F101L) in the catalytic domain. The mutant protein results in a higher MaK level and decreased expression of cartilage extracellular matrix genes and upregulation of inflammation-associated genes.
conclusionWe found that Sirt5-mediated MaK is an important regulator of chondrocyte cellular metabolism, and dysregulation of Sirt5-MaK could be an important mechanism underlying aging- and obesity-associated OA development.
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.