Autophagy and cartilage homeostasis mechanisms in joint health, aging and OA
Open accessAbstract
Osteoarthritis (OA) is the most prevalent joint disease, but neither preventive measures nor disease-modifying drugs are available and a continuing need exists for safe and effective symptom-modifying therapies. Clinical trials of candidate disease-modifying OA drugs in patients with established or advanced disease have not demonstrated their efficacy, but these failed trials have motivated investigation into the mechanisms that maintain joint health. The enhancement of such mechanisms could be a novel approach to reducing the risk of OA. Aging is one of the most important risk factors for OA; however, aging of joint cartilage is a process that is distinct from the subsequent cartilage changes that develop following the onset of OA. This Review focuses on the mechanisms that maintain cell and tissue homeostasis, and how these mechanisms fail during the aging process. Autophagy is a cellular homeostasis mechanism for the removal of dysfunctional organelles and macromolecules. Defective autophagy is involved in the pathogenesis of aging-related diseases and recent observations indicate that this process is compromised in aging cartilage. Augmentation of homeostasis mechanisms is discussed as a novel avenue to delay joint aging and reduce OA risk.
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Neither preventive measures nor disease-modifying treatments for osteoarthritis are yet available.
“for which disease-modifying treatments are not available”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [2]
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Platelet-rich plasma for managing pain and inflammation in osteoarthritis
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Effects of aging on articular cartilage homeostasis
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Biomarkers of Chondrocyte Apoptosis and Autophagy in Osteoarthritis
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“Autophagy can be inhibited by interleukins cleaved by Nod-like receptor protein 3 (NLRP3)-dependent caspase-1 [20,75,76].”
BackgroundWang, Y., Zhao, X., Lotz, M., Terkeltaub, R. A., & Liu‐Bryan, R. (2015) · Arthritis & Rheumatology · doi:10.1002/art.39182 · Cited by 303 · see citing works
“Factors that could induce and perpetuate a state of mitochondrial dysfunction in OA chondrocytes include the effects of nitric oxide, inflammation, oxidative stress, and other cell stresses on mitochondrial membrane polarization and oxidative phosphorylation and other functions, as well as persistent structural damage…”
BackgroundMesenchymal stem cell-based therapy of osteoarthritis: Current knowledge and future perspectives
Harrell, C. R., Marković, B. S., Fellabaum, C., Arsenijević, A., & Volarević, V. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.11.099 · Cited by 302 · see citing works
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“including miRNAs and by extracellular stimuli including cytokines, hormones and mechanical stress [7,8].”
BackgroundPost-traumatic osteoarthritis: from mouse models to clinical trials
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Self-citationCartilage tissue engineering: From biomaterials and stem cells to osteoarthritis treatments
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“To maintain homeostasis, chondrocytes depend predominantly on autophagic activity for removing damaged organelles or non-functional macromolecules [54].”
BackgroundMacro view of microRNA function in osteoarthritis
Miyaki, S., & Asahara, H. (2012) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2012.128 · Cited by 233 · see citing works
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Chondrosenescence: Definition, hallmarks and potential role in the pathogenesis of osteoarthritis
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“Autophagy may be a protective or homeostatic echanism in normal cartilage [22].”
BackgroundFGF signalling regulates bone growth through autophagy
Cinque, L., Forrester, A., Bartolomeo, R., Svelto, M., Venditti, R., Montefusco, S., Polishchuk, E., Nusco, E., Rossi, A., Medina, D. L., et al. (2015) · Nature · doi:10.1038/nature16063 · Cited by 199 · see citing works
The relationship of autophagy defects to cartilage damage during joint aging in a mouse model
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“health and may protect against OA (6).”
Intervertebral disc degeneration and osteoarthritis: a common molecular disease spectrum
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Autophagy Activation and Protection From Mitochondrial Dysfunction in Human Chondrocytes
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“Cellular homeostasis is dependent on intracellular mechanisms that maintain functional organelles and macromolecules required for cell survival and normal biosynthetic function (1).”
BackgroundBatushansky, A., Zhu, S., Komaravolu, R. K., South, S., Mehta-D’souza, P., & Griffin, T. M. (2021) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2021.06.013 · Cited by 177 · see citing works
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RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage
de Almeida, R. C., Ramos, Y. F., Mahfouz, A. E., den Hollander, W., Lakenberg, N., Houtman, E., van Hoolwerff, M., Suchiman, H. E. D., Ruiz, A. R., Slagboom, P. E., et al. (2019) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2018-213882 · Cited by 169 · see citing works
Emerging targets in osteoarthritis therapy
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“The loss of autophagy in articular cartilage under mechanical or inflammatory stress is linked to aging-related cell death and increasing OA severity [82,83].”
BackgroundProgranulin protects against osteoarthritis through interacting with TNF-α and β-Catenin signalling
Zhao, Y.-P., Liu, B., Tian, Q., Wei, J.-L., Richbourgh, B., & Liu, C.-J. (2014) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2014-205779 · Cited by 154 · see citing works
Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy
Nogueira-Recalde, U., Lorenzo-Gómez, I., Blanco, F. J., Loza, M. I., Grassi, D., Shirinsky, V., Shirinsky, I., Lotz, M., Robbins, P. D., Domínguez, E., et al. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2019.06.049 · Cited by 155 · see citing works
“OA is the most prevalent joint disease, and has a major impact on global health impact in the ageing population, but neither preventive measures nor disease-modifying treatments are yet available [2].”
BackgroundThe use of PRP injections in the management of knee osteoarthritis
O’Connell, B., Wragg, N. M., & Wilson, S. L. (2019) · Cell and Tissue Research · doi:10.1007/s00441-019-02996-x · Cited by 144 · see citing works
Autophagy: A new player in skeletal maintenance?
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“The role of autophagy in cartilage function has been recognized longer and is reviewed by Srinivas and colleagues(4) and Lotz and Caramés.”
BackgroundDysregulated FOXO transcription factors in articular cartilage in aging and osteoarthritis
Akasaki, Y., Hasegawa, A., Saito, M., Asahara, H., Iwamoto, Y., & Lotz, M. (2013) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2013.11.004 · Cited by 140 · see citing works
“were used to cut sections from the most proximal (1) to the most distal (6) location.”
MethodLiu, D., Cai, Z., Yang, Y.-T., Lu, W.-H., Pan, L.-Y., Xiao, W.-F., & Li, Y. (2021) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2021.10.009 · Cited by 137 · see citing works
Souza, R. B., Kumar, D., Calixto, N. E., Singh, J., Schooler, J., Subburaj, K., Li, X., Link, T. M., & Majumdar, S. (2014) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2014.04.017 · Cited by 134 · see citing works
p21 Both Attenuates and Drives Senescence and Aging in BubR1 Progeroid Mice
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“Aging is a complex biological process that increases the risk of a broad spectrum of human diseases and disorders, including diabetes, osteoporosis, arthritis, cataracts, sarcopenia, and cardiovascular and neurological disease (Campisi, 2005; Gau et al., 2011; Lotz and Caramés, 2011).”
Chen, L.-Y., Wang, Y., Terkeltaub, R. A., & Liu‐Bryan, R. (2018) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2018.07.004 · Cited by 127 · see citing works
“These include accumulation of DNA damage (3,4), and impairment of mitochondrial function (5,6), decrease in the autophagic process that normally removes damaged intracellular proteins and organelles (7), and deregulated nutrient biosensing, exemplified by decreased activity of the metabolic biosensor AMPK and of sever…”
BackgroundAging and the emerging role of cellular senescence in osteoarthritis
Diekman, B. O., & Loeser, R. F. (2023) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2023.11.018 · Cited by 130 · see citing works
Insulin decreases autophagy and leads to cartilage degradation
Ribeiro, M. P., de Figueroa, P. L., Blanco, F. J., Mendes, A. F., & Caramés, B. (2015) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2015.10.017 · Cited by 118 · see citing works
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“Autophagy is fundamental in maintaining chondrocyte homeostasis and adjusts cell metabolism in response to various stresses by removing damaged and unnecessary intracellular organelles and proteins (32).”
BackgroundAstaxanthin protects against osteoarthritis via Nrf2: a guardian of cartilage homeostasis
Sun, K., Luo, J.-H., Jing, X.-Z., Guo, J.-C., Yao, X., Hao, X.-X., Ye, Y.-P., Liang, S., Lin, J.-M., Wang, G.-C., et al. (2019) · Aging · doi:10.18632/aging.102474 · Cited by 70 · see citing works
“Cartilage degradation, caused by an imbalance in cartilage homeostasis, is a central feature of OA [4].”
BackgroundGlucosamine Activates Autophagy In Vitro and In Vivo
Caramés, B., Kiosses, W. B., Akasaki, Y., Brinson, D. C., Eap, W., Koziol, J. A., & Lotz, M. (2013) · Arthritis & Rheumatism · doi:10.1002/art.37977 · Cited by 96 · see citing works
JUNB‐FBXO21‐ERK axis promotes cartilage degeneration in osteoarthritis by inhibiting autophagy
Lin, Z., Miao, J., Zhang, T., He, M., Wang, Z.-Y., Feng, X., & Bai, L. (2021) · Aging Cell · doi:10.1111/acel.13306 · Cited by 89 · see citing works
“…the cross-regulation of spatial networks having multiple pathways and phenotypes such as ERK pathway, autophagy, apoptosis, anabolism, and catabolism (Glyn-Jones et al., 2015; Ji et al., 2019; Kim et al., 2014; Loeser et al., 2016; Lotz & Caramés, 2011; Rahmati et al., 2017; Zhang et al., 2017).”
BackgroundA comprehensive review on 3D tissue models: Biofabrication technologies and preclinical applications
Xie, R., Pal, V., Yu, Y., Lu, X., Gao, M., Liang, S., Huang, M., Peng, W., & Ozbolat, I. T. (2023) · Biomaterials · doi:10.1016/j.biomaterials.2023.122408 · Cited by 99 · see citing works
A Bi‐Lineage Conducive Scaffold for Osteochondral Defect Regeneration
Wu, Y., Zhu, S.-A., Wu, C.-T., Lu, P., Hu, C., Xiong, S., Chang, J., Heng, B.-O. C., Xiao, Y., & Ouyang, H. (2014) · Advanced Functional Materials · doi:10.1002/adfm.201304304 · Cited by 92 · see citing works
The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review
Luo, P., Gao, F., Niu, D., Sun, X., Song, Q., Guo, C., Liang, Y., & Sun, W. (2019) · BioMed Research International · doi:10.1155/2019/5171602 · Cited by 95 · see citing works
“The gradual accumulation of damaged macromolecules and organelles in somatic cells, which reduces the ability of cells to function and survive, is a core feature of aging-related diseases [15] .”
BackgroundOsteoarthritis year 2012 in review: biology
van der Kraan, P. M. (2012) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2012.07.010 · Cited by 94 · see citing works
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“As a negative regulator of inflammation, autophagy is thought to be a protective mechanism in normal cartilage, and decreased expression of key autophagy genes has been associated with increased apoptosis during OA development [37].”
BackgroundQin, N., Wei, L., Li, W., Yang, W., Cai, L., Qian, Z., & Wu, S. (2017) · Journal of Pharmacological Sciences · doi:10.1016/j.jphs.2017.06.002 · Cited by 93 · see citing works
CEMIP (KIAA1199) induces a fibrosis-like process in osteoarthritic chondrocytes
Deroyer, C., Charlier, E., Neuville, S., Malaise, O., Gillet, P., Kurth, W., Chariot, A., Malaise, M., & de Seny, D. (2019) · Cell Death and Disease · doi:10.1038/s41419-019-1377-8 · Cited by 91 · see citing works
Macroautophagy and aging: The impact of cellular recycling on health and longevity
Nieto-Torres, J. L., & Hansen, M. (2021) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2021.101020 · Cited by 91 · see citing works
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MicroRNA-155 suppresses autophagy in chondrocytes by modulating expression of autophagy proteins
D’Adamo, S., Álvarez-García, Ó., Muramatsu, Y., Flamigni, F., & Lotz, M. (2016) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2016.01.005 · Cited by 88 · see citing works
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Naringenin protects against iron overload-induced osteoarthritis by suppressing oxidative stress
Pan, Z., He, Q., Zeng, J., Li, S., Li, M., Chen, B., Yang, J., Xiao, J., Zeng, C., Luo, H., et al. (2022) · Phytomedicine · doi:10.1016/j.phymed.2022.154330 · Cited by 85 · see citing works
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mTOR: A Potential Therapeutic Target in Osteoarthritis?
Pal, B., Endisha, H., Zhang, Y., & Kapoor, M. (2015) · Drugs in R&D · doi:10.1007/s40268-015-0082-z · Cited by 82 · see citing works
“mTORC1 has been shown to associate with the ULK1Atg13-FIP200 complex, whereby it phosphorylates both ULK1 and Atg13, which represses ULK1 kinase activity [3, 78, 79].”
BackgroundJiang, L., Cao, L., Yin, X., Yasen, M., Yishake, M., Dong, J., & Li, X. (2015) · Cell Cycle · doi:10.1080/15384101.2015.1004946 · Cited by 82 · see citing works
“In osteoarthritis, autophagy is regarded as the principal mechanism responsible for cartilage and cellular homeostasis, although its negative and positive effect on osteoarthritis both have been reported.(35,36) Appropriate autophagy activation by rapamycin can even retard the progression of osteoarthritis in rats.”
BackgroundD’Adamo, S., Cetrullo, S., Guidotti, S., Silvestri, Y., Minguzzi, M., Santi, S., Cattini, L., Filardo, G., Flamigni, F., & Borzı̀, R. M. (2020) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2020.03.029 · Cited by 81 · see citing works
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“The exact causes of OA are unknown, but several risk factors have been identified, such as age, trauma, obesity, genetics, and other joint pathologies.(3) Inflammation is considered amajor factor associated with the risk of cartilage loss and OA perpetuation.”
BackgroundBach1 deficiency reduces severity of osteoarthritis through upregulation of heme oxygenase-1
Takada, T., Miyaki, S., Ishitobi, H., Hirai, Y., Nakasa, T., Igarashi, K., Lotz, M., & Ochi, M. (2015) · Arthritis Research & Therapy · doi:10.1186/s13075-015-0792-1 · Cited by 80 · see citing works
“Increased oxidative stress results from increased reactive oxygen species (ROS) generation and from reduced antioxidants, and is accompanied by a progressive accumulation of damaged molecules and organelles, leading to activation of catabolic factors such as inflammatory cytokines and extracellular matrix (ECM)-degrad…”
BackgroundMesenchymal stem cells (MSCs) as skeletal therapeutics–an update
Saeed, H., Ahsan, M., Saleem, Z., Iqtedar, M., Islam, M. F., Danish, Z., & Khan, A. M. (2016) · Journal of Biomedical Science · doi:10.1186/s12929-016-0254-3 · Cited by 77 · see citing works
“65 years of age demonstrating radiographic signs of diseased cartilage [87, 88].”
BackgroundPattappa, G., Johnstone, B., Zellner, J., Docheva, D., & Angele, P. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20030484 · Cited by 79 · see citing works
Osteoarthritis year in review 2023: Biology
Roelofs, A. J., & Bari, C. D. (2023) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2023.11.002 · Cited by 76 · see citing works
Zhang, H., Wang, H., Zeng, C., Yan, B., Ouyang, J., Liu, X., Sun, Q., Zhao, C., Fang, H., Pan, J., et al. (2017) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2016.12.024 · Cited by 74 · see citing works
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Álvarez-García, Ó., Fisch, K. M., Wineinger, N. E., Akagi, R., Saito, M., Sasho, T., Su, A. I., & Lotz, M. (2016) · Arthritis & Rheumatology · doi:10.1002/art.39643 · Cited by 75 · see citing works
“41 and 42).”
Zheng, W., Li, X., Liu, D., Li, J., Yang, S., Gao, Z., Wang, Z., Yokota, H., & Zhang, P. (2018) · The FASEB Journal · doi:10.1096/fj.201801851r · Cited by 74 · see citing works
“These data are consistent with previous reports in which autophagy is considered important for protection of cartilage homeostasis (31, 32).”
BackgroundResultWang, X., Qi, H., Wang, Q., Zhu, Y. J., Wang, X., Jin, M. Y., Tan, Q., Huang, Q., Xu, W., Li, X., et al. (2015) · Autophagy · doi:10.1080/15548627.2015.1091551 · Cited by 73 · see citing works
“Generally, autophagy promotes cell survival by providing nutrients to cells for adapting to stress conditions, and eliminating redundant, aging and defective proteins to maintain cellular homeostasis.(18) In growth plate, autophagy protects hypertrophic chondrocytes from apoptosis under the stress such as hypoxia and…”
BackgroundGuo, H., Yin, W., Zou, Z., Zhang, C., Sun, M., Min, L., Yang, L., & Kong, L. (2020) · Journal of Advanced Research · doi:10.1016/j.jare.2020.06.020 · Cited by 72 · see citing works
Recent Advances in Understanding the Role of Cartilage Lubrication in Osteoarthritis
Li, Y., Yuan, Z., Yang, H. L., Zhong, H., Peng, W., & Xie, R. (2021) · Molecules · doi:10.3390/molecules26206122 · Cited by 74 · see citing works
Biochemical Markers of Aging for Longitudinal Studies in Humans
Engelfriet, P. M., Jansen, E. H. J. M., Picavet, H. S. J., & Dollé, M. E. T. (2013) · Epidemiologic Reviews · doi:10.1093/epirev/mxs011 · Cited by 74 · see citing works
“Besides osteoporosis, osteoarthritis is among the most prevalent age-related diseases (150).”
BackgroundCetrullo, S., D’Adamo, S., Guidotti, S., Borzı̀, R. M., & Flamigni, F. (2016) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2016.03.002 · Cited by 72 · see citing works
“In fact defective autophagy has recently emerged as a feature of articular cartilage in OA-affected joints in both humans and animal models [3].”
BackgroundMicroRNA-146a Induced by Hypoxia Promotes Chondrocyte Autophagy through Bcl-2
Zhang, F., Wang, J., Chu, J., Yang, C., Xiao, H., Zhao, C., Sun, Z., Gao, X., Chen, G., Han, Z., et al. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000438513 · Cited by 68 · see citing works
Zhang, H., Zheng, W.-D., Li, D.-J., & Zheng, J. (2021) · Cartilage · doi:10.1177/19476035211023550 · Cited by 57 · see citing works
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Khan, N. M., Ansari, M. Y., & Haqqi, T. M. (2016) · Journal of Cellular Biochemistry · doi:10.1002/jcb.25750 · Cited by 62 · see citing works
“Earlier studies suggested that activation of autophagy appears to be beneficial in joint disease and protect against the development of OA [Lotz and Carames, 2011].”
BackgroundÁlvarez-García, Ó., Olmer, M., Akagi, R., Akasaki, Y., Fisch, K. M., Shen, T., Su, A. I., & Lotz, M. (2016) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2016.04.015 · Cited by 57 · see citing works
“Recent evidence supports a central role of autophagy in cartilage homeostasis and OA development 36 .”
BackgroundBNIP3-Dependent Mitophagy via PGC1α Promotes Cartilage Degradation
Kim, D., Song, J., & Jin, E.-J. (2021) · Cells · doi:10.3390/cells10071839 · Cited by 55 · see citing works
“Autophagy may play a crucial role in maintaining cartilage homeostasis and the deregulation of autophagy could contribute to cartilage degradation, a hallmark of OA pathogenesis [20].”
BackgroundLiu, Y., Zhu, H., Yan, X., Gu, H.-Y., Gu, Z., & Liu, F. (2017) · Biochemical and Biophysical Research Communications - BBRC · doi:10.1016/j.bbrc.2017.07.094 · Cited by 52 · see citing works
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ZHANG, Z. M., Shen, C., Li, H., FAN, Q., Ding, J., JIN, F. C., & Sha, L. (2016) · Molecular Medicine Reports · doi:10.3892/mmr.2016.4970 · Cited by 54 · see citing works
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Dhanabalan, K. M., Dravid, A. A., Agarwal, S., Sharath, R. K., Padmanabhan, A. K., & Agarwal, R. (2022) · Bioengineering & Translational Medicine · doi:10.1002/btm2.10298 · Cited by 53 · see citing works
“Autophagy is a stress survival mechanism that gets activated as an adaptive process to different forms of metabolic stress, and the role of autophagy in OA is widely studied.(8,12,15) Cellular senescence is another growing field and is an important target for many diseases, including OA.”
BackgroundLiao, S., Zheng, Q., Shen, H., Yang, G., Xu, Y., Zhang, X., Ouyang, H., & Pan, Z. (2022) · Arthritis & Rheumatology · doi:10.1002/art.42369 · Cited by 53 · see citing works
Chondrocyte Aging: The Molecular Determinants and Therapeutic Opportunities
Ramasamy, T. S., Yee, Y. M., & Khan, I. M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.625497 · Cited by 52 · see citing works
Shen, T., Álvarez-García, Ó., Li, Y.-K., Olmer, M., & Lotz, M. K. (2016) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2016.09.017 · Cited by 52 · see citing works
Jayaram, P., Yeh, P. C., Patel, S., Cela, R., Shybut, T. B., Grol, M. W., & Lee, B. (2019) · The American Journal of Sports Medicine · doi:10.1177/0363546519827294 · Cited by 52 · see citing works
“Importantly, although analysis of frozen aliquots of PRP was previously reported in the literature, this is more representative of platelet lysate.(1,2,4,9,10,18,19) While the literature cites meaningful information with the use of platelet lysates, it is not typically used in peripheral joint applications.”
BackgroundResultInfluentialNutraceutical Activity in Osteoarthritis Biology: A Focus on the Nutrigenomic Role
D’Adamo, S., Cetrullo, S., Panichi, V., Mariani, E., Flamigni, F., & Borzı̀, R. M. (2020) · Cells · doi:10.3390/cells9051232 · Cited by 52 · see citing works
“An additional pathway to counteract cartilage derangement is via the promotion of autophagy [39], i.”
BackgroundLee, D.-Y., Park, Y., Song, M.-G., Kim, D. R., Zada, S., & Kim, D. (2020) · Antioxidants · doi:10.3390/antiox9010083 · Cited by 50 · see citing works
FGF2: A Key Regulator Augmenting Tendon-to-Bone Healing and Cartilage Repair
Zhang, J., Liu, Z., Li, Y., You, Q., Yang, J., Jin, Y. H., Zou, G., Tang, J., Ge, Z., & Liu, Y. (2020) · Regenerative Medicine · doi:10.2217/rme-2019-0080 · Cited by 49 · see citing works
Integrin signalling in joint development, homeostasis and osteoarthritis
Miao, M. Z., Lee, J. S., Yamada, K. M., & Loeser, R. F. (2024) · Nature Reviews Rheumatology · doi:10.1038/s41584-024-01130-8 · Cited by 48 · see citing works
Zhao, X., Li, H., & Wang, L. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.03.005 · Cited by 48 · see citing works
RetractedDefective autophagy in chondrocytes with Kashin-Beck disease but higher than osteoarthritis
Wu, C., Zheng, J., Yao, X., Shan, H., Li, Y., Xu, P., & Guo, X. (2014) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2014.08.010 · Cited by 47 · see citing works
Jiang, L., Lee, S., Wang, Y., Xu, Q., Meng, D., & Zhang, J. (2016) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2015.12.021 · Cited by 46 · see citing works
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D’Adamo, S., Cetrullo, S., Minguzzi, M., Silvestri, Y., Borzı̀, R. M., & Flamigni, F. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/3720128 · Cited by 45 · see citing works
“Autophagy failure contributes to OA pathogenesis and is responsible for the accumulation of cellular defects in chondrocytes [11, 12].”
BackgroundRole of TLR2 and TLR4 in regulation of articular chondrocyte homeostasis
Wang, Y., Zhao, X., & Liu‐Bryan, R. (2020) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2020.01.011 · Cited by 44 · see citing works
“autophagy have been shown to involve in regulation of chondrocyte homeostasis, and their dysfunction is associated with OA (9,10), we studied the cellular stress responses in chondrocytes deficient in TLR2 and TLR4 in vitro.”
BackgroundCai, H., Wang, P., Yang, X., Yao, Y. D., Liu, J., Li, T., Sun, Y., Liang, J., Fan, Y., & Zhang, X. (2019) · Regenerative Biomaterials · doi:10.1093/rb/rbz028 · Cited by 44 · see citing works
“PCs would endow the cartilage with a certain capacity for self-renewal under mechanical abrasion [6, 7].”
BackgroundInfluentialBhattacharjee, M., Ivirico, J. L. E., Kan, H.-M., Bordett, R., Pandey, R., Otsuka, T., Nair, L. S., & Laurencin, C. T. (2020) · Scientific Reports · doi:10.1038/s41598-020-75921-w · Cited by 44 · see citing works
- Authors
- Lotz, M. K., & Caramés, B.
- Affiliations
- Scripps Research Institute (US)
- Corresponding author
- Lotz, Martin K.
- Venue
- Nature Reviews Rheumatology
- Published
- 2011-08-02
- Volume
- 7
- Issue
- 10
- Pages
- 579-587
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- PMC
- PMC3192496
- OpenAlex
- W1985004392
- Cited by
- 314
- References
- 99
- Citations by year
- 2026: 15 · 2025: 18 · 2024: 32 · 2023: 27 · 2022: 27 · 2021: 27 · 2020: 29 · 2019: 23 · 2018: 14 · 2017: 13 · 2016: 20 · 2015: 19 · 2014: 16 · 2013: 20 · 2012: 11
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P01AG007996, AG-007996)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR056026, R01AR056026)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Surgery › Hip disorders and treatments
- Keywords
- autophagy, cartilage homeostasis, osteoarthritis, joint aging, cartilage aging, disease-modifying osteoarthritis drugs, joint health, age-related diseases
- MeSH terms
- Aging, Animals, Autophagy, Cartilage, Articular, Homeostasis, Humans, Osteoarthritis
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