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学者姓名：武淑芳
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Abstract ：
Peripheral neuropeptide Y (NPY) has been reported to regulate bone metabolism and homeostasis; however, its potential roles in growth plate chondrogenesis remain unclear. Here, we found that NPY expression decreased during chondrocyte differentiation in vitro and in vivo. NPY was required for chondrocyte proliferation; in contrast, knockdown of NPY facilitated chondrocyte hypertrophic differentiation. Administration of recombinant NPY in rat chondrocytes and metatarsal bones uncoupled normal proliferation and hypertrophic differentiation during chondrogenesis and thereby inhibited growth plate chondrogenesis and longitudinal bone growth. Remarkably, NPY activated the mTORC1 pathway in chondrocytes, whereas attenuation of mTORC1 activity by administration of rapamycin in vitro partially abrogated NPY-mediated effects on chondrocyte proliferation and hypertrophic differentiation. In addition, a combination of Y2R antagonist but not Y1R antagonist with NPY abolished NPY-mediated inhibition of metatarsal growth and growth plate chondrogenesis. Mechanistically, NPY activated Erk1/2 by NPY2R, then phosphorylated ERK1/2 activated mTORC1 to initiate PTHrP expression, which in turn promoted chondrocyte proliferation and inhibited chondrocyte hypertrophic differentiation. In conclusion, our data identified NPY as a crucial regulator of chondrogenesis and may provide a promising therapeutic strategy for skeletal diseases.
Keyword ：
chondrocytes hypertrophic differentiation mTORC1 NPY proliferation
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| GB/T 7714 | Kang, Xiaomin , Ma, Xiao , Li, Huixia et al. Neuropeptide Y Promotes mTORC1 to Regulate Chondrocyte Proliferation and Hypertrophy [J]. | ENDOCRINOLOGY , 2023 , 164 (3) . |
| MLA | Kang, Xiaomin et al. "Neuropeptide Y Promotes mTORC1 to Regulate Chondrocyte Proliferation and Hypertrophy" . | ENDOCRINOLOGY 164 . 3 (2023) . |
| APA | Kang, Xiaomin , Ma, Xiao , Li, Huixia , Jin, Xinxin , Gao, Xin , Feng, Dongxu et al. Neuropeptide Y Promotes mTORC1 to Regulate Chondrocyte Proliferation and Hypertrophy . | ENDOCRINOLOGY , 2023 , 164 (3) . |
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Abstract ：
Obesity is closely associated with low-bone-mass disorder. Discoidin domain receptor 2 (DDR2) plays essential roles in skeletal metabolism, and is probably involved in fat metabolism. To test the potential role of DDR2 in fat and fat-bone crosstalk, Ddr2 conditional knockout mice (Ddr2(Adipo)) were generated in which Ddr2 gene is exclusively deleted in adipocytes by Adipoq Cre. We found that Ddr2(Adipo) mice are protected from fat gain on high-fat diet, with significantly decreased adipocyte size. Ddr2(Adipo) mice exhibit significantly increased bone mass and mechanical properties, with enhanced osteoblastogenesis and osteoclastogenesis. Marrow adipocyte is diminished in the bone marrow of Ddr2(Adipo) mice, due to activation of lipolysis. Fatty acid in the bone marrow was reduced in Ddr2(Adipo) mice. RNA-Seq analysis identified adenylate cyclase 5 (Adcy5) as downstream molecule of Ddr2. Mechanically, adipocytic Ddr2 modulates Adcy5-cAMP-PKA signaling, and Ddr2 deficiency stimulates lipolysis and supplies fatty acid for oxidation in osteoblasts, leading to the enhanced osteoblast differentiation and bone mass. Treatment of Adcy5 specific inhibitor abolishes the increased bone mass gain in Ddr2(Adipo) mice. These observations establish, for the first time, that Ddr2 plays an essential role in the crosstalk between fat and bone. Targeting adipocytic Ddr2 may be a potential strategy for treating obesity and pathological bone loss simultaneously.
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| GB/T 7714 | Yang, Xiaoyu , Li, Jing , Zhao, Liting et al. Targeting adipocytic discoidin domain receptor 2 impedes fat gain while increasing bone mass [J]. | CELL DEATH AND DIFFERENTIATION , 2021 , 29 (4) : 737-749 . |
| MLA | Yang, Xiaoyu et al. "Targeting adipocytic discoidin domain receptor 2 impedes fat gain while increasing bone mass" . | CELL DEATH AND DIFFERENTIATION 29 . 4 (2021) : 737-749 . |
| APA | Yang, Xiaoyu , Li, Jing , Zhao, Liting , Chen, Yazhuo , Cui, Zhijun , Xu, Taotao et al. Targeting adipocytic discoidin domain receptor 2 impedes fat gain while increasing bone mass . | CELL DEATH AND DIFFERENTIATION , 2021 , 29 (4) , 737-749 . |
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Abstract ：
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Keyword ：
Autophagosome cancer flux LC3 lysosome macroautophagy neurodegeneration phagophore stress vacuole
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| GB/T 7714 | Klionsky, Daniel J. , Abdel-Aziz, Amal Kamal , Abdelfatah, Sara et al. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) [J]. | AUTOPHAGY , 2021 , 17 (1) : 1-382 . |
| MLA | Klionsky, Daniel J. et al. "Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)" . | AUTOPHAGY 17 . 1 (2021) : 1-382 . |
| APA | Klionsky, Daniel J. , Abdel-Aziz, Amal Kamal , Abdelfatah, Sara , Abdellatif, Mahmoud , Abdoli, Asghar , Abel, Steffen et al. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) . | AUTOPHAGY , 2021 , 17 (1) , 1-382 . |
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Abstract ：
It has been established that excessive apoptosis of nucleus pulposus cells (NPCs) are responsible for pathogenesis of human intervertebral disc degeneration (IDD). The present study aimed to shed light on the molecular mechanisms underlying the protective effects of mesenchymal stem cells (MSCs) on NPCs in an inflammatory environment. NPCs were treated with TNF-α to induce inflammation and then co-cultured with Wharton's Jelly-derived MSCs (WJ-MSCs)without direct interaction. The levels of inflammation markers (IL-1β, IL-6 and IL-8) in NPCs were detected by performing enzyme-linked immunosorbent assay (ELISA), and expression of metalloproteases and aggrecan, as well as the activity of p38 MAPK pathway were determined through immunoblotting. SB-203580 was used to inhibit p38 signaling, prior to evaluation of the effects of Wharton's Jelly-derived MSCs (WJ-MSCs) on inflammatory response within the co-cultured NPCs. After TNF-α treatment, the levels of inflammatory cytokines, MMP-3, and MMP-13 in NPCs were increased whereas aggrecan was decreased, which was then dramatically reversed by WJ-MSCs co-culture. Likewise, WJ-MSCs suppressed TNF-α-induced phosphorylation of p38 MAPK signaling components including p38, ASK-1, MKK-3 and MKK-6. Blocking p38 MAPK pathway enhanced the anti-inflammatory impact of WJ-MSCs, and there was no significant difference between NPCs co-cultured with WJ-MSCs or the cells cultured alone. WJ-MSCs co-culture mitigate TNF-α-induced inflammatory response and ECM degeneration in NPCs, the major pathological events are implicated in IDD development, probably by suppressing the p38 MAPK signaling cascade.
Keyword ：
anti-inflammation intervertebral disc degeneration mesenchymal stromal cell p38/MAPK
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| GB/T 7714 | Zhao Yuanting , Qin Yue , Wu Shufang et al. Mesenchymal stem cells regulate inflammatory milieu within degenerative nucleus pulposus cells via p38 MAPK pathway. [J]. | Experimental and therapeutic medicine , 2020 , 20 (5) : 22 . |
| MLA | Zhao Yuanting et al. "Mesenchymal stem cells regulate inflammatory milieu within degenerative nucleus pulposus cells via p38 MAPK pathway." . | Experimental and therapeutic medicine 20 . 5 (2020) : 22 . |
| APA | Zhao Yuanting , Qin Yue , Wu Shufang , Huang Dageng , Hu Huimin , Zhang Xinliang et al. Mesenchymal stem cells regulate inflammatory milieu within degenerative nucleus pulposus cells via p38 MAPK pathway. . | Experimental and therapeutic medicine , 2020 , 20 (5) , 22 . |
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Abstract ：
A large number of studies in recent years indicated the involvement of peripheral circadian clock in varied pathologies. However, evidence regarding how peripheral clocks regulate bone metabolism is still very limited. The present study aimed to investigate the direct role of Bmal1 (the key activator of peripheral circadian clock system) in vivo during bone developmental and remodeling stages using inducible osteoblast-specific Bmal1 knockout mice. Unexpectedly, the removal of Bmal1 in osteoblasts caused multiple abnormalities of bone metabolism, including a progressive increase in trabecular bone mass in as early as 8 weeks, manifested by an 82.3% increase in bone mineral density and 2.8-fold increase in bone volume per tissue volume. As mice age, an increase in trabecular bone mass persists while cortical bone mass decreases by about 33.7%, concomitant with kyphoscoliosis and malformed intervertebral disk. The increased trabecular bone mass is attributed to increased osteoblast number and osteoblast activity coupled with decreased osteoclastogenesis. Remarkably, the ablation of Bmal1 in osteoblasts promoted the expression level of Bmp2 and phosphorylation of SMAD1, whereas the attenuation of BMP2/SMAD1 signaling partially alleviated the effects of Bmal1 deficiency on osteoblast differentiation and activity. The results revealed that Bmal1 was a transcriptional silencer of Bmp2 by targeting the Bmp2 promoter. The peripheral clock gene Bmal1 in osteoblasts was crucial to coordinate differential effects on trabecular and cortical bones through regulating BMP2/SMAD1 during bone development, thus providing novel insights into a key role of osteoblast Bmal1 in homeostasis and integrity of adult bones. This article is protected by copyright. All rights reserved.
Keyword ：
Bmal1 BMP2/p-SMAD1 kyphoscoliosis osteoblasts
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| GB/T 7714 | Qian Zhuang , Zhang Ying , Kang Xiaomin et al. Postnatal conditional deletion of Bmal1 in osteoblasts enhances trabecular bone formation via increased BMP2 signals. [J]. | Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research , 2020 , 35 (8) : 1481-1493 . |
| MLA | Qian Zhuang et al. "Postnatal conditional deletion of Bmal1 in osteoblasts enhances trabecular bone formation via increased BMP2 signals." . | Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 35 . 8 (2020) : 1481-1493 . |
| APA | Qian Zhuang , Zhang Ying , Kang Xiaomin , Li Huixia , Zhang Yan , Jin Xinxin et al. Postnatal conditional deletion of Bmal1 in osteoblasts enhances trabecular bone formation via increased BMP2 signals. . | Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research , 2020 , 35 (8) , 1481-1493 . |
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Abstract ：
Sirt1 involved in cellular aging and aging-related diseases, including osteoarthritis (OA). Our previous study showed Sirt1 played a role in the pathogenesis of OA, however, the underlying mechanisms are still poorly elicited. In this study, we investigated the role of Sirt1 in epigenetically regulating P53/P21 pathway in a Sirt1 loss model. Sirt1 deletion male mice (n = 10) with destabilization of the medial meniscus (DMM) were used to observe its role on OA development. Then, the relationships between SIRT1 and P53 were detected by Coimmunoprecipitation (ColP), and the gain-off function of P53 gene was indicated by P53 activators and inhibitors in vitro. Finally, human cartilage samples from patients with OA were collected. Sirt1 deletion mice displayed a spontaneous OA development, manifesting severe chondrocytes hypertrophy markers MMP13 and ADAMTS5, highly expressed P53 and P21. Strikingly, surgery-induced meniscus injury promoted the OA pathogenesis and apoptosis in Sirt1 deficient mice. Ultimately, our ColP data demonstrated that Sirt1 directly interacted with P53 in vitro. However inhibition of P53 alleviated OA progression. We also observed that chondrocyte apoptosis and P53 increased in osteoarthritis (OA) progression with a declining expression of Sirt1 in human cartilage. Loss of Sirt1 in cartilage led to accelerated OA pathogenesis via aberrant activation of p53/p21 mediated senescence associated secretory phenotype, hypertrophy and apoptosis. (C) 2020 Elsevier Inc. All rights reserved.
Keyword ：
Apoptosis Epigenetic regulation Osteoarthritis P53 Sirt1 deletion
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| GB/T 7714 | Xu, Mao , Feng, Meng , Peng, Hang et al. Epigenetic regulation of chondrocyte hypertrophy and apoptosis through Sirt1/P53/P21 pathway in surgery-induced osteoarthritis [J]. | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS , 2020 , 528 (1) : 179-185 . |
| MLA | Xu, Mao et al. "Epigenetic regulation of chondrocyte hypertrophy and apoptosis through Sirt1/P53/P21 pathway in surgery-induced osteoarthritis" . | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 528 . 1 (2020) : 179-185 . |
| APA | Xu, Mao , Feng, Meng , Peng, Hang , Qian, Zhuang , Zhao, Liting , Wu, Shufang . Epigenetic regulation of chondrocyte hypertrophy and apoptosis through Sirt1/P53/P21 pathway in surgery-induced osteoarthritis . | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS , 2020 , 528 (1) , 179-185 . |
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Abstract ：
Progranulin (PGRN) is an autocrine growth factor that exerts crucial roles within cartilage tissue; however, the molecular mechanisms underlying PGRN-mediated cartilage homeostasis remain elusive. In the present study, we investigated the role of PGRN in regulating chondrocyte homeostasis and its therapeutic potential for managing osteoarthritis (OA). We found that PGRN levels are significantly increased in human cartilage in mild OA and that its expression is decreased in the cartilage in severe OA. In vitro, treatment of primary rat chondrocytes with recombinant PGRN significantly enhanced the levels of collagen type II a 1 chain (COL2A1) and aggrecan, and attenuated TNFa-induced up-regulation of matrix metallopeptidase 13 (MMP13) and ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) in chondrocytes. These effects were abrogated in SIRT12/2 cells, indicating a causative role of SIRT1 in the effects of PGRN on protein expression in chondrocytes. Mechanistically, PGRN increased SIRT1 expression and activity, which reduced the acetylation levels of SRY-box transcription factor (SOX9) and transcription factor P65 (P65) and thereby promoted nuclear translocation of SOX9 and inhibited TNFa-induced P65 nuclear accumulation to maintain chondrocyte homeostasis. In conclusion, our findings reveal a mechanism of action for PGRN that maintains cartilage homeostasis and supports the notion that PGRN up-regulation may be a promising strategy for managing OA. © 2020 Feng et al. Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc.
Keyword ：
Acetylation Cartilage Tissue homeostasis Transcription Transcription factors
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| GB/T 7714 | Feng, Dongxu , Kang, Xiaomin , Wang, Ruiqi et al. Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65 [J]. | Journal of Biological Chemistry , 2020 , 295 (39) : 13640-13650 . |
| MLA | Feng, Dongxu et al. "Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65" . | Journal of Biological Chemistry 295 . 39 (2020) : 13640-13650 . |
| APA | Feng, Dongxu , Kang, Xiaomin , Wang, Ruiqi , Chen, He , Zhang, Kun , Feng, Weilou et al. Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65 . | Journal of Biological Chemistry , 2020 , 295 (39) , 13640-13650 . |
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Abstract ：
Progranulin (PGRN) is an autocrine growth factor that exerts crucial roles within cartilage tissue; however, the molecular mechanisms underlying PGRN-mediated cartilage homeostasis remain elusive. In the present study, we investigated the role of PGRN in regulating chondrocyte homeostasis and its therapeutic potential for managing osteoarthritis (OA). We found that PGRN levels are significantly increased in human cartilage in mild OA and that its expression is decreased in the cartilage in severe OA. In vitro, treatment of primary rat chondrocytes with recombinant PGRN significantly enhanced the levels of collagen type II α 1 chain (COL2A1) and aggrecan, and attenuated TNFα-induced up-regulation of matrix metallopeptidase 13 (MMP13) and ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) in chondrocytes. These effects were abrogated in SIRT1-/- cells, indicating a causative role of SIRT1 in the effects of PGRN on protein expression in chondrocytes. Mechanistically, PGRN increased SIRT1 expression and activity, which reduced the acetylation levels of SRY-box transcription factor (SOX9) and transcription factor P65 (P65) and thereby promoted nuclear translocation of SOX9 and inhibited TNFα-induced P65 nuclear accumulation to maintain chondrocyte homeostasis. In conclusion, our findings reveal a mechanism of action for PGRN that maintains cartilage homeostasis and supports the notion that PGRN up-regulation may be a promising strategy for managing OA.
Keyword ：
cartilage chondrocytes deacetylation growth factor inflammation joint disease osteoarthritis PGRN progranulin SIRT1 sirtuin 1
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| GB/T 7714 | Feng Dongxu , Kang Xiaomin , Wang Ruiqi et al. Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65. [J]. | The Journal of biological chemistry , 2020 , 295 (39) : 13640-13650 . |
| MLA | Feng Dongxu et al. "Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65." . | The Journal of biological chemistry 295 . 39 (2020) : 13640-13650 . |
| APA | Feng Dongxu , Kang Xiaomin , Wang Ruiqi , Chen He , Zhang Kun , Feng Weilou et al. Progranulin modulates cartilage-specific gene expression via sirtuin 1-mediated deacetylation of the transcription factors SOX9 and P65. . | The Journal of biological chemistry , 2020 , 295 (39) , 13640-13650 . |
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Abstract ：
Excessive inflammatory response-induced apoptosis and the degeneration of articular chondrocytes contribute to the development and progression of osteoarthritis. PDZ and LIM domain containing protein 2 (PDLIM2) has emerged as one of the pivotal regulators in orchestrating an inflammatory response through regulating the activity of transcription factor nuclear factor (NF)-κB. However, whether PDLIM2 participates in the articular chondrocyte-associated inflammatory response in osteoarthritis remains unknown. In the current study, we aimed to explore the biological function of PDLIM2 in lipopolysaccharide (LPS)-stimulated articular chondrocytes, an in vitro model of osteoarthritis. Herein, we found that PDLIM2 expression was significantly down-regulated in chondrocytes in response to LPS exposure. Functional experiments revealed that PDLIM2 overexpression increased the viability and decreased the apoptosis of chondrocytes following LPS treatment. Moreover, PDLIM2 overexpression attenuated LPS-induced degeneration of chondrocytes via the down-regulation of matrix metalloproteinase (MMP)-3 and MMP-13 and the up-regulation of COL2A1 and ACAN. In addition, the overexpression of PDLIM2 decreased LPS-induced production of interleukin (IL)-1β, IL-6 and TNF-α. In contrast, depletion of PDLIM2 exhibited the opposite effect. Mechanism research elucidated that PDLIM2 repressed the activation of NF-κB signaling associated with the down-regulation of NF-κB p65 protein expression. PDLIM2 depletion-exacerbated LPS-induced injury was significantly reversed by NF-κB inhibition. Taken together, these results demonstrate that PDLIM2 overexpression attenuates LPS-induced injury of articular chondrocytes through the inactivation of NF-κB signaling.
Keyword ：
Chondrocyte Inflammation NF-κB Osteoarthritis PDLIM2
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| GB/T 7714 | Guo Qinyue , Xu Jing , Shi Qindong et al. PDLIM2 protects articular chondrocytes from lipopolysaccharide-induced apoptosis, degeneration and inflammatory injury through down-regulation of nuclear factor (NF)-κB signaling. [J]. | International immunopharmacology , 2020 , 88 : 106883 . |
| MLA | Guo Qinyue et al. "PDLIM2 protects articular chondrocytes from lipopolysaccharide-induced apoptosis, degeneration and inflammatory injury through down-regulation of nuclear factor (NF)-κB signaling." . | International immunopharmacology 88 (2020) : 106883 . |
| APA | Guo Qinyue , Xu Jing , Shi Qindong , Wu Shufang . PDLIM2 protects articular chondrocytes from lipopolysaccharide-induced apoptosis, degeneration and inflammatory injury through down-regulation of nuclear factor (NF)-κB signaling. . | International immunopharmacology , 2020 , 88 , 106883 . |
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Abstract ：
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic destructive joint disease. To date, the etiology and pathogenesis of RA have not been fully elucidated, but a large number of studies have indicated that hypoxia is an important feature of RA. Our study was designed to probe how hypoxia-induced exosome (exo) derived from synovial fibroblasts (SFs) affect RA. In this study, we found that hypoxic environment existed in synovial tissue of RA, and miR-424 expression was increased in RA, and exosome derived from synovial fibroblasts (SFs-exo) could significantly induce T cells differentiation, which Th17 cells increased and Treg cells decreased. Besides, SFs-exo affected the expression of related inflammatory cytokines. And, we also found that FOXP3 was a target gene of miR-424 and exo-miR-424 KD inhibited RA worsening. These results suggested that SFs-exo in hypoxia aggravates rheumatoid arthritis by regulating Treg/Th17 balance and thus may be a potential therapeutic target for RA. Impact statement A comparative study of osteoarthritis (OA) and RA mice was implemented to suggest that miR-424 expression was increased in RA, and exosome-miR-424 derived from synovial fibroblasts (SFs-exo) could significantly induce T cells differentiation in which Th17 cells increased and Treg cells decreased via targeting FOXP3. And thus, miR-424 may be a potential therapeutic target for RA.
Keyword ：
exosome Hypoxia rheumatoid arthritis Th17 Treg cells
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| GB/T 7714 | Ding, Yanjie , Wang, Laifang , Wu, Huiqiang et al. Exosomes derived from synovial fibroblasts under hypoxia aggravate rheumatoid arthritis by regulating Treg/Th17 balance [J]. | EXPERIMENTAL BIOLOGY AND MEDICINE , 2020 , 245 (14) : 1177-1186 . |
| MLA | Ding, Yanjie et al. "Exosomes derived from synovial fibroblasts under hypoxia aggravate rheumatoid arthritis by regulating Treg/Th17 balance" . | EXPERIMENTAL BIOLOGY AND MEDICINE 245 . 14 (2020) : 1177-1186 . |
| APA | Ding, Yanjie , Wang, Laifang , Wu, Huiqiang , Zhao, Qing , Wu, Shufang . Exosomes derived from synovial fibroblasts under hypoxia aggravate rheumatoid arthritis by regulating Treg/Th17 balance . | EXPERIMENTAL BIOLOGY AND MEDICINE , 2020 , 245 (14) , 1177-1186 . |
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