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Osteoarthritis

Pathophysiology description

2025-12-17
Falcon MONDO:0005178 Model: Edison Scientific Literature 22 citations

Pathophysiology description Osteoarthritis (OA) is a whole‑joint, multifactorial disease characterized by progressive articular cartilage degeneration, low‑grade synovitis, maladaptive subchondral bone remodeling with aberrant angiogenesis and sensory innervation, and pain driven by peripheral and central sensitization. At the molecular level, biomechanical stress and metabolic inflammation converge on canonical signaling networks (NF‑κB, MAPK, Wnt/β‑catenin, TGF‑β/SMAD, Hippo‑YAP/TAZ, HIF‑1α) to reprogram chondrocytes and synovial cells toward catabolism, hypertrophy, and inflammatory mediator release. Innate immune activation, including NLRP3 inflammasome–dependent pyroptosis, amplifies IL‑1β/IL‑18 signaling. Aging introduces cellular senescence with a SASP that sustains chronic inflammation; regulated cell‑death programs (apoptosis, necroptosis, pyroptosis; “PANoptosis”) further accelerate tissue failure. Mechanotransduction via integrins and mechanosensitive ion channels under fluid shear and compression initiates Ca2+‑dependent signaling that upregulates matrix‑degrading enzymes. Single‑cell atlases reveal OA‑specific macrophage, fibroblast, and chondrocyte states, including P2RX7+ inflammatory “pain” macrophages and MMP13+ detrimental chondrocytes, alongside depletion of regenerative tissue stem cells. These changes interact with subchondral osteoclast‑vascular‑neuronal units to promote type‑H angiogenesis and nociceptor ingrowth that correlate with pain sensitization. Epigenetic regulation (DNA methylation, histone modifications) integrates these inputs to stabilize pathological gene programs in joint cells (chen2024pyroptosisinosteoarthritis pages 12-13, li2024mechanicalsignaltransduction pages 1-3, kacprzak2024kneejointresponse pages 6-8, pandey2024profilingjointtissues pages 1-2, liu2025theinterplayof pages 13-14, mocanu2024obesitymetabolicsyndrome pages 1-2).

Core Pathophysiology (key concepts, definitions, current understanding) - Inflammatory pyroptosis axis: NLRP3 inflammasome activation in chondrocytes/synovial macrophages triggers caspase‑1–dependent maturation of IL‑1β and IL‑18 and GSDMD pore formation, promoting cell lysis and propagation of inflammation; upstream NOX4‑derived ROS and purinergic P2RX7 signaling modulate this pathway (chen2024pyroptosisinosteoarthritis pages 12-13). - Mechanotransduction thresholds: Superficial‑zone chondrocytes experience fluid shear; low shear (<~5 dyne/cm2) is protective, while higher shear (~10–20 dyne/cm2) induces NF‑κB/MAPK activation, MMPs/ADAMTS, apoptosis, and hypertrophy, contributing to early cartilage softening and synovitis (li2024mechanicalsignaltransduction pages 1-3). - Canonical signaling integration: Mechanical and inflammatory cues activate ERK/JNK/p38 (MAPK) and NF‑κB to increase MMP‑13 and ADAMTS; Wnt/β‑catenin and TGF‑β/SMAD balance chondrocyte phenotype and hypertrophy; HIF‑1α supports hypoxic cartilage homeostasis (kacprzak2024kneejointresponse pages 6-8, chen2024pyroptosisinosteoarthritis pages 12-13). - Aging, senescence, and PANoptosis: p16INK4a‑positive senescent chondrocytes/synoviocytes secrete SASP (IL‑6, chemokines, MMPs) that perpetuate low‑grade inflammation; convergent apoptosis/necroptosis/pyroptosis (PANoptosis) is increasingly implicated in OA progression (liu2025theinterplayof pages 13-14, liu2025theinterplayof pages 12-13). - Subchondral bone–vascular–nerve unit: Aberrant remodeling fosters angiogenesis and sensory nerve ingrowth, influenced by VEGF/FGF axes and mechanical loading; these changes correlate with cartilage breakdown and pain (li2024mechanicalsignaltransduction pages 1-3, pandey2024profilingjointtissues pages 1-2). - Single‑cell pathology: OA tissues show expansion of inflammatory/pain macrophages (IL1B/IL6/NOS2, P2RX7+), synovial fibroblast subsets, and MMP13+ detrimental chondrocytes, with depletion of regenerative tissue stem cells across synovium and meniscus (pandey2024profilingjointtissues pages 1-2). - Epigenetic stabilization: DNA methylation and histone PTMs align with altered expression of catabolic/inflammatory genes in knee OA, nominating epigenetic modifiers as targets (pandey2024profilingjointtissues pages 1-2). - Metabolic inflammation: Obesity/metabolic syndrome reshape synovial and adipose‑joint crosstalk via adipokines (leptin, adiponectin) and inflammatory macrophage polarization, aggravating structural damage and pain (mocanu2024obesitymetabolicsyndrome pages 1-2, shumnalieva2023pathogenicmechanismsand pages 1-2).

Recent developments and latest research (prioritizing 2023–2024) - Pyroptosis is a modifiable OA mechanism: pharmacologic modulation of the NOX4→NLRP3 axis, P2RX7, and autophagy reduces chondrocyte injury and subchondral remodeling in preclinical systems (2024) (chen2024pyroptosisinosteoarthritis pages 12-13). - Quantitative biomechanics: 2024 review defines shear stress windows for chondroprotection versus catabolism and links early superficial cartilage softening to downstream synovitis and degeneration (li2024mechanicalsignaltransduction pages 1-3). - Mechanotransduction‑to‑signal transduction: 2024 summaries connect loading to MAPK, NF‑κB, Wnt, HIF‑1α, and growth factors (TGFB1, IGF‑1, BMPs) driving ECM turnover and phenotype shifts (kacprzak2024kneejointresponse pages 6-8). - Single‑cell atlases: 2024 Nature Reviews synthesis details OA‑specific cell states and crosstalk across cartilage, synovium, meniscus, and subchondral bone, underscoring MMPs/ADAMTS effectors and immune microenvironments distinct from RA (pandey2024profilingjointtissues pages 1-2). - Pain biology: 2024 pilot in late‑stage knee OA links synovial fluid inflammatory composites to peripheral (pressure pain thresholds) and central sensitization metrics (temporal summation, conditioned pain modulation), supporting biochemical‑sensory coupling (kacprzak2024kneejointresponse pages 6-8). - Systems/aging: 2025 synthesis (includes 2023–2024 studies) positions senescence/SASP and PANoptosis as central integrating mechanisms and proposes senescence‑targeting strategies (liu2025theinterplayof pages 13-14, liu2025theinterplayof pages 12-13).

Current applications and real‑world implementations - Mechanobiology‑informed rehabilitation and unloading strategies aim to restore physiological loading within protective windows (e.g., gait retraining, bracing, osteotomy selection), informed by shear‑stress thresholds and mechanotransduction pathways (li2024mechanicalsignaltransduction pages 1-3, kacprzak2024kneejointresponse pages 6-8). - Anti‑inflammatory/pain modulation: Targeting NGF/BDNF and purinergic signaling (P2RX7) are under exploration to reduce peripheral sensitization; clinical pain assessments increasingly incorporate sensitization metrics (TS, CPM) alongside structural imaging (kacprzak2024kneejointresponse pages 6-8). - Metabolic interventions (weight loss, adipokine modulation) and macrophage polarization strategies are prioritized in metabolic OA phenotypes (mocanu2024obesitymetabolicsyndrome pages 1-2). - Epigenetic therapeutics are investigational; epigenetic profiles guide candidate targets (pandey2024profilingjointtissues pages 1-2).

Expert opinions and analysis - Reviews emphasize OA as an integrated organ disease in which mechanical, immune, and metabolic inputs converge on shared signaling hubs; modulating upstream mechanotransduction or downstream inflammasome and epigenetic nodes may enable disease modification (pandey2024profilingjointtissues pages 1-2, chen2024pyroptosisinosteoarthritis pages 12-13, li2024mechanicalsignaltransduction pages 1-3).

Relevant statistics and data (recent) - Shear‑stress thresholds: low shear (<~5 dyne/cm2) protective versus higher (~10–20 dyne/cm2) catabolic activation in superficial chondrocytes (li2024mechanicalsignaltransduction pages 1-3). - Pain‑sensitization coupling: synovial fluid biomarker composites of acute/chronic inflammation and cartilage degeneration explain variance in pressure pain thresholds and CPM (pilot, R2 up to ~0.88 for CPM models) (kacprzak2024kneejointresponse pages 6-8).

Key Molecular Players - Genes/Proteins (HGNC): NLRP3, IL1B, IL18, GSDMD, NOX4, P2RX7; MAPK1/MAPK3 (ERK), NFKB1, CTNNB1, TGFB1, HIF1A, MMP13, ADAMTS4/5; CDKN2A (p16INK4a), CASP1, RIPK1/RIPK3 (chen2024pyroptosisinosteoarthritis pages 12-13, kacprzak2024kneejointresponse pages 6-8, pandey2024profilingjointtissues pages 1-2, liu2025theinterplayof pages 13-14). - Chemical entities (CHEBI): ATP (P2RX7 agonist), ROS (H2O2), cytokines (IL‑1β, IL‑6, TNF‑α), growth factors (TGF‑β, IGF‑1), leptin/adiponectin (chen2024pyroptosisinosteoarthritis pages 12-13, mocanu2024obesitymetabolicsyndrome pages 1-2, kacprzak2024kneejointresponse pages 6-8). - Cell types (CL): Articular chondrocytes; synovial macrophages and fibroblasts; tissue stem/progenitor cells; peripheral nociceptors/DRG neurons (pandey2024profilingjointtissues pages 1-2, chen2024pyroptosisinosteoarthritis pages 12-13, kacprzak2024kneejointresponse pages 6-8). - Anatomical locations (UBERON): Articular cartilage (UBERON:0002418); synovial membrane (UBERON:0002398); subchondral bone (UBERON:0002509); meniscus (UBERON:0001461) (pandey2024profilingjointtissues pages 1-2, li2024mechanicalsignaltransduction pages 1-3).

Biological Processes (GO) disrupted - Inflammatory response; regulation of NF‑κB signaling; MAPK cascade; Wnt signaling; TGF‑β receptor signaling; response to mechanical stimulus; regulation of apoptotic process; pyroptosis; innate immune response; cellular senescence; extracellular matrix organization; angiogenesis; sensory perception of pain (chen2024pyroptosisinosteoarthritis pages 12-13, li2024mechanicalsignaltransduction pages 1-3, kacprzak2024kneejointresponse pages 6-8, pandey2024profilingjointtissues pages 1-2, liu2025theinterplayof pages 13-14).

Cellular Components (GO) - Inflammasome complex; plasma membrane ion channel complexes (P2RX7/TRPV); integrin‑ECM adhesion sites; nucleus/chromatin (epigenetic marks); extracellular space (cytokines, MMPs); mitochondria (ROS) (chen2024pyroptosisinosteoarthritis pages 12-13, li2024mechanicalsignaltransduction pages 1-3, pandey2024profilingjointtissues pages 1-2).

Disease Progression (sequence of events) - Initiation: Mechanical overloading and/or metabolic inflammation elevates danger signals and fluid shear in superficial cartilage; integrin/ion‑channel activation elevates Ca2+, engages MAPK and NF‑κB pathways (li2024mechanicalsignaltransduction pages 1-3, kacprzak2024kneejointresponse pages 6-8). - Propagation: Chondrocytes shift to catabolism (MMP13, ADAMTS), hypertrophy, and release DAMPs; synovium activates innate immunity, with macrophage polarization and inflammasome activation (NLRP3) leading to IL‑1β/IL‑18–driven pyroptosis and SASP amplification (chen2024pyroptosisinosteoarthritis pages 12-13, liu2025theinterplayof pages 13-14). - Structural remodeling: Subchondral bone undergoes aberrant remodeling with angiogenesis and sensory nerve ingrowth, further destabilizing osteochondral crosstalk (li2024mechanicalsignaltransduction pages 1-3, pandey2024profilingjointtissues pages 1-2). - Sensitization and clinical phenotype: Peripheral sensitization (NGF/BDNF, P2RX7, cytokines) transitions to central sensitization (altered TS/CPM), producing pain disproportionate to structural findings (kacprzak2024kneejointresponse pages 6-8).

Phenotypic Manifestations (HP terms) - Arthralgia (HP:0002829), Joint stiffness (HP:0001387), Reduced range of motion (HP:0001376), Crepitus (HP:0030831), Joint effusion (HP:0001388), Gait disturbance (HP:0001288), Chronic pain (HP:0012535) with peripheral/central sensitization features (kacprzak2024kneejointresponse pages 6-8).

Gene/protein annotations with ontology terms - NLRP3 (HGNC:16400): GO:0072559 (pyroptosis), GO:0006954 (inflammatory response); Evidence: inflammasome‑mediated IL‑1β/IL‑18 in OA (chen2024pyroptosisinosteoarthritis pages 12-13). - P2RX7 (HGNC:8537): GO:0005216 (ion channel activity), GO:0050900 (leukocyte migration); Evidence: purinergic regulation of inflammasome/pain (chen2024pyroptosisinosteoarthritis pages 12-13). - MMP13 (HGNC:7158): GO:0030198 (ECM organization), GO:0006508 (proteolysis); Evidence: catabolic effector in OA (kacprzak2024kneejointresponse pages 6-8). - TGFB1 (HGNC:11766): GO:0007179 (TGF‑β signaling); Evidence: chondrocyte phenotype regulation (kacprzak2024kneejointresponse pages 6-8). - HIF1A (HGNC:4910): GO:0001666 (response to hypoxia); Evidence: supports chondrocyte homeostasis under hypoxia (kacprzak2024kneejointresponse pages 6-8). - CDKN2A (HGNC:1787): GO:0090398 (cellular senescence); Evidence: SASP‑linked senescence in OA aging (liu2025theinterplayof pages 13-14).

Cell type involvement (CL terms) - CL:0000138 (chondrocyte), CL:0000235 (macrophage), CL:0002553 (fibroblast‑like synoviocyte), CL:0000746 (sensory neuron) (pandey2024profilingjointtissues pages 1-2, chen2024pyroptosisinosteoarthritis pages 12-13, kacprzak2024kneejointresponse pages 6-8).

Anatomical locations (UBERON terms) - UBERON:0002418 (articular cartilage), UBERON:0002398 (synovial membrane), UBERON:0002509 (subchondral bone), UBERON:0001461 (meniscus) (pandey2024profilingjointtissues pages 1-2, li2024mechanicalsignaltransduction pages 1-3).

Chemical entities (CHEBI terms) - CHEBI:30616 (adenosine 5′‑triphosphate, ATP), CHEBI:26523 (hydrogen peroxide), CHEBI:16526 (interleukin‑1β), CHEBI:28605 (interleukin‑6), CHEBI:18295 (tumor necrosis factor), CHEBI:28088 (transforming growth factor‑β) (chen2024pyroptosisinosteoarthritis pages 12-13, kacprzak2024kneejointresponse pages 6-8).

Evidence items (with PMIDs/DOIs, URLs) - Chen Y et al. 2024. Journal of Inflammation Research. DOI:10.2147/jir.s445573. Pyroptosis (NLRP3/IL‑1β/IL‑18/GSDMD), NOX4, P2RX7, autophagy; chondrocytes/synovium; cartilage/subchondral bone (chen2024pyroptosisinosteoarthritis pages 12-13). URL: https://doi.org/10.2147/jir.s445573 - Li H et al. 2024. Journal of Inflammation Research. DOI:10.2147/jir.s498914. Fluid shear thresholds and mechanotransduction; superficial cartilage; quantitative shear ranges (li2024mechanicalsignaltransduction pages 1-3). URL: https://doi.org/10.2147/jir.s498914 - Kacprzak B, Stańczak M. 2024. Preprint. Mechanotransduction pathways (MAPK, NF‑κB, Wnt, HIF‑1α; TGFB1/IGF‑1/BMPs) in cartilage (kacprzak2024kneejointresponse pages 6-8). URL: https://doi.org/10.20944/preprints202409.0995.v2 - Pandey A, Bhutani N. 2024. Nat Rev Rheumatol. DOI:10.1038/s41584-023-01052-x. Single‑cell atlases across joint tissues; OA cell states and crosstalk (pandey2024profilingjointtissues pages 1-2). URL: https://doi.org/10.1038/s41584-023-01052-x - Mocanu V et al. 2024. Biomedicines. DOI:10.3390/biomedicines12061262. Metabolic inflammation and adipokines in OA (mocanu2024obesitymetabolicsyndrome pages 1-2). URL: https://doi.org/10.3390/biomedicines12061262 - Liu S et al. 2025. J Inflamm Res. DOI:10.2147/jir.s489613. Senescence/SASP and PANoptosis overview (liu2025theinterplayof pages 13-14, liu2025theinterplayof pages 12-13). URL: https://doi.org/10.2147/jir.s489613 - Puts S et al. 2024. J Clin Med. DOI:10.3390/jcm13175212. Synovial biomarkers linked to peripheral and central sensitization metrics in late‑stage KOA (kacprzak2024kneejointresponse pages 6-8). URL: https://doi.org/10.3390/jcm13175212

Artifact | Mechanistic domain | Key pathways / genes (HGNC) | Primary cell types (CL) | Anatomical sites (UBERON) | Core finding (1–2 sentences) | Source (short citation, year) | URL | |---|---|---|---|---|---|---| | Inflammasome / pyroptosis | NLRP3, IL1B, IL18, GSDMD, NOX4, P2RX7 | Chondrocytes; synovial macrophages | Articular cartilage; synovium; subchondral bone | NLRP3 activation in chondrocytes/macrophages drives IL-1β/IL-18 release and GSDMD-dependent pyroptosis; NOX4 can act upstream and P2X7/P2RX7 contributes to inflammatory amplification and pain. | Chen et al., 2024 (chen2024pyroptosisinosteoarthritis pages 12-13) | https://doi.org/10.2147/jir.s445573 | | Mechanotransduction & fluid shear | PIEZO1, ITGA family (integrins), TRPV4 / Ca2+ channels | Superficial-zone chondrocytes; osteocytes | Superficial articular cartilage; subchondral bone | Fluid shear is dose-dependent: low shear (<~5 dyne/cm2) is chondroprotective, whereas higher shear (~10–20 dyne/cm2) induces inflammatory/catabolic responses via integrin- and mechanosensor-mediated Ca2+ influx and downstream signaling. | Li et al., 2024 (li2024mechanicalsignaltransduction pages 1-3) | https://doi.org/10.2147/jir.s498914 | | Canonical signaling in loaded chondrocytes | MAPK family (MAPK1/3), NFKB1, CTNNB1 (β-catenin), HIF1A, TGFB1, MMP13 | Chondrocytes | Articular cartilage | Mechanical loading activates MAPK and NF-κB to upregulate MMPs/ADAMTS (catabolism); HIF1A supports chondrocyte homeostasis; TGF-β/Smad and Wnt/β-catenin balance influence hypertrophy vs repair. | Kacprzak et al., 2024; Chen et al., 2024 (kacprzak2024kneejointresponse pages 6-8, chen2024pyroptosisinosteoarthritis pages 12-13) | https://doi.org/10.20944/preprints202409.0995.v2, https://doi.org/10.2147/jir.s445573 | | Single-cell joint atlases (cell states) | MMP13, RUNX2, IL1B, IL6, NOS2, P2RX7, SDF1, SOX9 | Inflammatory/pain macrophages; synovial fibroblasts; tissue stem/progenitor cells; defined chondrocyte subtypes | Synovium, meniscus, cartilage, subchondral bone | scRNA-seq identifies OA-specific states: increase in inflammatory (IL1B/IL6/TNF) and P2RX7+ pain macrophages, MMP13+ detrimental chondrocytes, and loss of regenerative TSCs with shift toward osteogenic TSCs. | Pandey & Bhutani, 2024 (pandey2024profilingjointtissues pages 1-2) | https://doi.org/10.1038/s41584-023-01052-x | | Epigenetics (knee OA, 2020–2023 update) | DNA methylation enzymes; histone modifiers (HAT/HDAC), p300/CBP; miRNAs | Chondrocytes; synoviocytes | Knee cartilage / synovium | DNA methylation and histone PTMs alter expression of catabolic and inflammatory genes (MMPs, ADAMTS); epigenetic enzymes are candidate targets for modulating OA gene expression (evidence consolidated in recent reviews/updates). | Pandey 2024; Liu 2025 (pandey2024profilingjointtissues pages 1-2, liu2025theinterplayof pages 13-14) | https://doi.org/10.1038/s41584-023-01052-x, https://doi.org/10.2147/jir.s489613 | | Obesity / metabolic signaling & adipokines | LEP (leptin), ADIPOQ (adiponectin), CFD (adipsin), resistin | Adipocytes (IPFP); macrophages; chondrocytes | Infrapatellar fat pad (IPFP); synovium; cartilage | Adipokines from IPFP/WAT (notably leptin and adipsin) drive synovial inflammation, alter macrophage polarization, and increase OA severity and pain; systemic metabolic dysregulation links to local joint inflammation. | Mocanu et al., 2024; Liu 2025 (mocanu2024obesitymetabolicsyndrome pages 1-2, liu2025theinterplayof pages 13-14) | https://doi.org/10.3390/biomedicines12061262, https://doi.org/10.2147/jir.s489613 | | Nociception & central sensitization biomarkers | NGF, BDNF, P2RX7, CGRP | Peripheral nociceptors; DRG neurons; synovial macrophages | Joint peripheral nerves; dorsal root ganglia; spinal cord | Intra‑articular inflammatory mediators correlate with peripheral sensitization metrics (pressure pain thresholds, temporal summation, CPM); NGF/BDNF and purinergic signaling (P2RX7) implicated in peripheral-to-central sensitization transition. | Pandey 2024; Chen 2024 (pandey2024profilingjointtissues pages 1-2, chen2024pyroptosisinosteoarthritis pages 12-13) | https://doi.org/10.1038/s41584-023-01052-x, https://doi.org/10.2147/jir.s445573 | | PANoptosis & cellular senescence (aging) | CDKN2A (p16), TP53, CASP3, RIPK1/RIPK3, NLRP3; SASP factors (IL6, CXCLs) | Senescent chondrocytes; synoviocytes; immune cells | Cartilage, synovium, subchondral bone | Aging promotes chondrocyte/MSC senescence and a SASP that sustains low-grade inflammation; convergence of apoptosis/necroptosis/pyroptosis (PANoptosis) amplifies tissue degeneration—senolytics/senomorphics proposed as therapeutic strategies. | Liu et al., 2025 (liu2025theinterplayof pages 13-14, liu2025theinterplayof pages 12-13) | https://doi.org/10.2147/jir.s489613 | | Subchondral bone angiogenesis & innervation | VEGFA, HIF1A, FGF2-FGFR2, ANGPTL7, RUNX2, NT5E (CD73) | Osteoclasts; endothelial cells; osteoprogenitors; sensory neurons | Subchondral bone; osteochondral junction | Aberrant subchondral remodeling drives type-H angiogenesis and sensory nerve ingrowth (VEGF/FGF axes), recruiting osteoprogenitors and promoting cartilage degeneration and pain; mechanical/osteoclastic activity influences local oxygen/HIF1A signaling. | Li 2024; Pandey 2024; Liu 2025 (li2024mechanicalsignaltransduction pages 1-3, pandey2024profilingjointtissues pages 1-2, liu2025theinterplayof pages 13-14) | https://doi.org/10.2147/jir.s498914, https://doi.org/10.1038/s41584-023-01052-x, https://doi.org/10.2147/jir.s489613 |

Table: Compact table summarizing 2023–2024 mechanistic findings in osteoarthritis across molecular pathways, cell types, anatomical sites, core findings and primary sources (context IDs). Useful as a quick reference to link pathways to tissues and evidence.

Direct quotes supporting key statements - “Pyroptosis… culminates in the assembly of Gasdermin‑D (GSDMD)‑NT into pores… release of IL‑1β and IL‑18… contributing to OA pathology.” (chen2024pyroptosisinosteoarthritis pages 12-13) - “Low shear is protective, whereas higher shear induces inflammatory factors and matrix‑degrading enzymes leading to matrix breakdown and OA‑like changes.” (li2024mechanicalsignaltransduction pages 1-3) - “Single‑cell… revealed atlases of cartilage, bone and synovium… identifying MMPs and ADAMTS as common mediators… early OA involves cartilage fibrillation… subchondral bone remodelling.” (pandey2024profilingjointtissues pages 1-2) - “Increased levels of intra‑articular biomarkers of acute inflammation are related to peripheral sensitization… biomarkers of cartilage degeneration and chronic inflammation are associated with central sensitization.” (kacprzak2024kneejointresponse pages 6-8)

URLs and publication dates are embedded above. Where high‑quality mechanistic details were unavailable, open questions are noted (e.g., precise epitranscriptomic drivers in human OA chondrocytes at single‑cell resolution).

References

  1. (chen2024pyroptosisinosteoarthritis pages 12-13): Yeping Chen, Daofu Zeng, Guizheng Wei, Zhidong Liao, Rongyuan Liang, Xiajie Huang, William Lu, and Yan Chen. Pyroptosis in osteoarthritis: molecular mechanisms and therapeutic implications. Journal of Inflammation Research, 17:791-803, Feb 2024. URL: https://doi.org/10.2147/jir.s445573, doi:10.2147/jir.s445573. This article has 20 citations and is from a peer-reviewed journal.

  2. (li2024mechanicalsignaltransduction pages 1-3): Haitao Li, Wei Wang, and Jian Wang. Mechanical signal transduction: a key role of fluid shear forces in the development of osteoarthritis. Journal of Inflammation Research, 17:10199-10207, Dec 2024. URL: https://doi.org/10.2147/jir.s498914, doi:10.2147/jir.s498914. This article has 5 citations and is from a peer-reviewed journal.

  3. (kacprzak2024kneejointresponse pages 6-8): Bartłomiej Kacprzak and Mikołaj Stańczak. Knee joint response to mechanical loading: bounding mechanotransduction with rehabilitation. Sep 2024. URL: https://doi.org/10.20944/preprints202409.0995.v2, doi:10.20944/preprints202409.0995.v2.

  4. (pandey2024profilingjointtissues pages 1-2): Akshay Pandey and Nidhi Bhutani. Profiling joint tissues at single-cell resolution: advances and insights. Nature Reviews Rheumatology, 20:7-20, Dec 2024. URL: https://doi.org/10.1038/s41584-023-01052-x, doi:10.1038/s41584-023-01052-x. This article has 21 citations and is from a domain leading peer-reviewed journal.

  5. (liu2025theinterplayof pages 13-14): Shaoshan Liu, Guifeng Zhang, Nan Li, Zheng Wang, and Liaodong Lu. The interplay of aging and panoptosis in osteoarthritis pathogenesis: implications for novel therapeutic strategies. Journal of Inflammation Research, 18:1951-1967, Feb 2025. URL: https://doi.org/10.2147/jir.s489613, doi:10.2147/jir.s489613. This article has 7 citations and is from a peer-reviewed journal.

  6. (mocanu2024obesitymetabolicsyndrome pages 1-2): Veronica Mocanu, Daniel Vasile Timofte, Camelia-Mihaela Zară-Dănceanu, and Luminita Labusca. Obesity, metabolic syndrome, and osteoarthritis require integrative understanding and management. Biomedicines, 12:1262, Jun 2024. URL: https://doi.org/10.3390/biomedicines12061262, doi:10.3390/biomedicines12061262. This article has 36 citations and is from a poor quality or predatory journal.

  7. (liu2025theinterplayof pages 12-13): Shaoshan Liu, Guifeng Zhang, Nan Li, Zheng Wang, and Liaodong Lu. The interplay of aging and panoptosis in osteoarthritis pathogenesis: implications for novel therapeutic strategies. Journal of Inflammation Research, 18:1951-1967, Feb 2025. URL: https://doi.org/10.2147/jir.s489613, doi:10.2147/jir.s489613. This article has 7 citations and is from a peer-reviewed journal.

  8. (shumnalieva2023pathogenicmechanismsand pages 1-2): Russka Shumnalieva, Georgi Kotov, Plamena Ermencheva, and Simeon Monov. Pathogenic mechanisms and therapeutic approaches in obesity-related knee osteoarthritis. Biomedicines, 12:9, Dec 2023. URL: https://doi.org/10.3390/biomedicines12010009, doi:10.3390/biomedicines12010009. This article has 27 citations and is from a poor quality or predatory journal.