2022
DOI: 10.1016/j.nantod.2021.101367
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Nanoengineered therapy aiming at the etiology of rheumatoid arthritis

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Cited by 25 publications
(13 citation statements)
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“…Considering the central role of M1 macrophages in the pathogenesis of RA, efficient repolarization of M1 macrophages to the anti-inflammatory M2 phenotype has become a viable strategy for RA treatment. For instance, Wen Zhou et al proposed that silver nanoparticles could target M1 macrophages via the folic acid (FA) receptor to reprogram their polarization state . Interestingly, recent insights increasingly reveal that the elevated ROS production in M1 macrophages is a multifaceted driver of RA pathophysiology . On one hand, due to their high biochemical reactivity, the abundant ROS would elicit severe damage to the DNA and proteins to cause cellular injury and cartilage damage. On the other hand, it could also regulate the TLR/nuclear factor κB (NF-κB) activation in M1 macrophages to amplify the inflammation. Consequently, normalizing the redox homeostasis in M1 macrophages could yield complementary benefits for RA treatment, which may not only reduce the ROS-mediated direct tissue damage but also reprogram them into anti-inflammatory M2 phenotypes to treat inflammatory diseases. , …”
Section: Introductionmentioning
confidence: 99%
“…Considering the central role of M1 macrophages in the pathogenesis of RA, efficient repolarization of M1 macrophages to the anti-inflammatory M2 phenotype has become a viable strategy for RA treatment. For instance, Wen Zhou et al proposed that silver nanoparticles could target M1 macrophages via the folic acid (FA) receptor to reprogram their polarization state . Interestingly, recent insights increasingly reveal that the elevated ROS production in M1 macrophages is a multifaceted driver of RA pathophysiology . On one hand, due to their high biochemical reactivity, the abundant ROS would elicit severe damage to the DNA and proteins to cause cellular injury and cartilage damage. On the other hand, it could also regulate the TLR/nuclear factor κB (NF-κB) activation in M1 macrophages to amplify the inflammation. Consequently, normalizing the redox homeostasis in M1 macrophages could yield complementary benefits for RA treatment, which may not only reduce the ROS-mediated direct tissue damage but also reprogram them into anti-inflammatory M2 phenotypes to treat inflammatory diseases. , …”
Section: Introductionmentioning
confidence: 99%
“…Therefore, the HNV might act as a nanosponge to absorb inflammatory factors and reduce the inflammatory response. 40 Accordingly, the potential binding capability of HNV@BP to IL-6 or TNF-α, which play prominent roles in initiating and promoting the progression of RA, was tested by enzyme-linked immunosorbent assay (ELISA). As shown in Fig.…”
Section: Resultsmentioning
confidence: 99%
“…[272][273][274] Given the pathological features of RA, incorporating contrast agents or drugs into nanomaterials to design nanoprobes or nanodrugs can not only improve drugresponsive release capability but also provide visual information on pathological features and improve therapeutic outcome. [275][276][277][278][279][280] For example, Wang et al developed an inflammation-induced disassembly nanoplatform (DCNR-MTX-CPs/siRNA) wherein conjugated polymer NPs (CPs) were combined with down-conversion nanorods (DCNRs) via bisulfide bridges and then modified using siRNA (Figure 17A). [281] NIR-II FL signal was initially quenched because of the Forster resonance energy transfer (FRET) effect between CPs and DCNRs.…”
Section: Biomarker-responsive Nanotheranostics For Rheumatoid Arthritismentioning
confidence: 99%