Cause Of Rheumatoid Arthritis Research Articles

The recent progress of γδ T cells and its targeted therapies in rheumatoid arthritis.

Rheumatoid arthritis (RA) is an autoimmune condition that mostly impacts the joints. During the advanced phases of the disorder, it may be accompanied by other problems. While the precise cause of RA is uncertain, various research has been conducted to gain a better understanding of the immunological processes involved in the development of RA. T cells are acknowledged as significant contributors to the progression of RA because of their roles in cytokine secretion, antigen presentation, and facilitating B cells in the manufacture of antibodies. γδ T cells are a small subset of T cells that have significant functions in the context of infection and diseases linked with tumors. γδ T cells have been the subject of investigation in autoimmune disorders in recent years. This review focused on the involvement of γδ T lymphocytes in the development of RA. In this article, we provide an analysis of the immunological capabilities of γδ T cells, intending to comprehend their significance in RA, which could be pivotal in the creation of innovative clinical treatments.

Mechanism of PD-1/PD-L1 in Regulating cTfr/cTfh Balance in Patients with Rheumatoid Arthritis

Rheumatoid arthritis (RA) is frequent, an imbalance between helper cells (Th) and regulatory T cells (Treg) is the fundamental immunological cause of RA. This study investigates how recombinant human programmed cell death 1 (PD-L1) protein affects circulating T follicular helper (cTfh), circulating T follicular regulatory (cTfr), and their equilibrium. Magnetic bead sorting was used to select CD4+CXCR5+T cells from RA patients' and healthy individuals' peripheral blood mononuclear cells for in vitro growth. Recombinant human PD-L1 protein stimulated CD4+CXCR5+T cells. Cell counting kit 8 (CCK-8), flow cytometry surface labeling, ELISA, and RT-PCR were used to measure CD4+CXCR5+T cell proliferation inhibition, cTfh and cTfr frequencies, IL-21 expression, and PI3K, AKT, Bcl-6, and Blimp-1 mRNA levels. The recombinant human PD-L1 protein dose-dependently inhibited the proliferation of CD4+CXCR5+T cells in active RA peripheral blood. However, it has a weaker inhibitory effect on healthy peripheral blood CD4+CXCR5+T cells. PD-L1 protein decreased cTfh in active RA peripheral blood CD4+CXCR5+T overall cultured cells but did not affect cTfr; The cTfr/cTfh ratio increased but did not affect the frequency of cTfh and cTfr in healthy persons' cultured CD4+CXCR5+T cells. PD-L1 protein reduced IL-21 in CD4+CXCR5+T cell culture supernatant from active RA peripheral blood. Recombinant human PD-L1 protein lowered PI3K, AKT, and Bcl-6 mRNA in active RA peripheral blood CD4+CXCR5+T cell culture, including significant differences. But Blinmp-1 mRNA variations were neither substantial nor statistically different. PD-1/PD-L1 limits cTfh proliferation, differentiation, and activation via the PI3K/AKT signaling pathway regulates its immunological balance with cTfr, and corrects the cTfr/cTfh imbalance by controlling their interaction.

RNA-seq Based Transcriptome Analysis Reveals Role of Myoglobin in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease which manifests as joint destruction and bone erosion, could be caused by both genetic and environmental factors. Currently, the causes of RA are unknown, and targeted therapies are often associated with side effects and contraindications. The detection rate of RA in women is higher than men (3:1), however, there is still a lack of comprehensive understanding of the relationship between sex and RA. We hypothesized gender differences in RA prevalence and their associated mechanisms by performing genome-wide transcriptome analysis of synovial biopsy samples. The results indicated that myoglobin (MB) was differentially expressed between males and females, with higher expression in males than females in healthy populations, while the opposite was observed in RA patients. MB interacted with HLA class II histocompatibility antigen, DM beta (HLA-DMB) and the inflammatory factor interleukin 6 (IL-6) in the human synovial cell line MH7A.

Knowledge and Attitudes of General Population's Toward Rheumatoid Arthritis in Hail, Saudi Arabia

Background: A chronic inflammatory autoimmune illness, rheumatoid arthritis (RA) mainly affects small, symmetrical joints, especially those in the hand, wrist, and foot. However, it can also affect other joints and systems. Joint deformity, persistent pain, and a reduced quality of life are brought on by recurrent assaults. Aim: The objective of the research is to evaluate the general public's awareness and insights regarding rheumatoid arthritis in Hail, Saudi Arabia. Method: The cross-sectional research took place on people in Hail who were at least 18 years old and over. A self-administered questionnaire was distributed among Hail population using online platforms primarily social media. The questionnaire includes basic demographic characteristics, types of RA, the causes of RA, the symptoms, the risk factors, complications, treatment of RA and whether they know what RA is or not. Results: 532 people in responded to the questionnaire; of them, 42.5% were female and 50.9% were male. 8.3% had received a diagnosis of RA, and 60.0% correctly associated it with joint pain and morning stiffness. 67.3% believed that RA is not a contagious disease. A significant majority (56.6%) correctly identified that women are more likely to develop RA. Regarding risk factors, 28.0% acknowledged smoking as a significant factor. A notable finding is that 63.7% were uncertain about RA's impact on pregnancy. Knowledge about specific joint involvement varied, with 60.0% correctly associating RA with inflammation in small joints. Conclusion: The results indicate that while some participants demonstrated a correct comprehension of the disease, there were misconceptions, particularly regarding the joint pain characteristic, types of joint involvement and extra-articular manifestations. These results emphasize how crucial it is to set educational initiatives in place to clear up these misunderstandings and raise community understanding about rheumatoid arthritis.

Mesenchymal Stem Cells and Curcumin Effectively Mitigate Freund's Adjuvant- induced Arthritis via their Anti-inflammatory and Gene Expression of COX-1, IL-6 and IL-4.

Rheumatoid arthritis (RA) is a type of arthritis that damages joints and can affect the thymus and the spleen. RA is an autoimmune disorder in which the immune system targets the body's own tissues. The causes of RA are unknown, although a genetic link is thought to be involved. The objective of this research was to evaluate the effect of curcumin, mesenchymal stem cells (MSCs), and their combination on the disruption of serum cytokines, ankle joint, thymus and spleen histopathology, and affected genes in complete Freund's adjuvant (CFA)-induced arthritis in male and female Wistar rats. Experimental animals were organized into 16 groups (6 animals for each), eight groups including male rats and the other eight groups including females rats. The groups are normal control, CMC, curcumin, MSCs, CFA, CFA/curcumin, CFA/ MSCs and the arthritic group treated with MSCs and curcumin. One subcutaneous injection of 0.1 mL CFA was given to rats into the right hind leg footpad to induce RA. The arthritic rats were intravenously injected three times with bone marrow-derived MSCs (BM-MSCs) and/or treated orally with curcumin daily (100 mg per kg body weight per day) for 21 days. Curcumin and BM-MSCs work together to dramatically (P < 0.05) restore the high serum PGE2 and IL-17 levels and lower the IL-13 level in arthritic rats to normal levels. Deleterious effects on the spleen and thymus histological structure were counteracted. Gene expression of COX-1 and IL-6 was increased and IL-4 was decreased; these changes were improved by the combination treatment (P < 0.05). Based on these findings, additive therapeutic effects on RA occur from the combined treatment of curcumin and BM-MSCs compared with their individual use (P < 0.05). Thus, it can be said that both curcumin and BM-MSCs are effective at reducing inflammation while also having beneficial effects on the ankle joint, thymus and spleen.

Current Prospects in Rheumatoid Arthritis: Pathophysiology, Genetics, and Treatments.

An autoimmune inflammatory disease, rheumatoid arthritis (RA), predominantly affects the synovium joint lining, augmenting disability, early mortality, and socioeconomic difficulty. Therefore, current updates on pharmacological therapies are crucial for developing drugs to treat the disease at each stage. This review attempts to compile a thorough analysis of current developments in our knowledge of RA pathogenesis and disease-modifying drugs, with the aim of providing insights for next-generation RA therapeutics. According to the literature, the most successful drugs for treatment techniques described so far in this include (cs) DMARDs (sub-class of DMARDs), tsDMARDS (targeted synthetic DMARDS), and bDMARDs (biological DMARDs). However, current pharmacologic therapy (consisting of biological, conventional, and creative views of small molecule anti-rheumatic drugs that treat the disease or DMARD) remains the cornerstone of rheumatoid arthritis treatment with which significant progress toward disease remission has been accomplished. The pathobiology of RA involves cytokine messengers such as B and T-cells, and an intricate interplay of pro-inflammatory cytokines responsible for activating and developing effector cells, in turn, accountable for local disease and systemic symptoms. Despite the fact that the cause of rheumatoid arthritis is not known, new treatments have been created as a result of better approaches towards the biology of the disease. As they target molecules directly implicated in the genesis of rheumatoid arthritis, these drugs may be more effective, targeted, and less harmful in the short and long term than standard therapies.

Therapeutic Effects of IL-1RA, M2 Cells, and Their Synergistic Impact on a Mouse Model of Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a type of autoimmune disease that results in chronic inflammation of the joint synovial tissue, leading to joint damage and significant disability. Despite ongoing research, the exact cause of RA remains unclear, and current treatments have limitations. This study explores the potential of utilizing interleukin-1 receptor antagonist (IL-1RA) and anti-inflammatory macrophages polarized in the vicinity of the supernatant from allogeneic mesenchymal stem cells (MSCs) as a novel therapeutic approach for RA. An expression cassette containing the IL-1RA gene was constructed and expressed in E. coli BL21. The resulting protein was purified and stabilized for use in in vivo experiments. Bone marrow MSCs were isolated and used to produce anti-inflammatory M2 macrophages from the isolated peripheral blood monocytes. The macrophages were then used to treat mice with RA induced by collagen type II. The combination of IL-1RA and M2 macrophages improved clinical and histopathological symptoms of the disease, reduced levels of inflammatory factors, and modulated the immune system in the treated mouse groups. The results showed that this combinatory therapy had a synergistic effect for RA treatment. The simultaneous use of IL-1RA and M2 cells could be a promising approach for the treatment of RA. This combinatory therapy has the potential to improve the disease and decrease the severity of inflammation in patients with RA.

Evaluation of the efficacy and safety of a herbal formulation for rheumatoid arthritis – A non-inferiority randomized controlled trial

Ethnopharmacological relevanceRheumatoid arthritis (RA) is a diverse disease characterized by a variable, progressive course of articular and extra-articular symptoms that are linked with pain, disability, and mortality. The exact cause of rheumatoid arthritis is still being investigated, and there is no cure for this debilitating, persistent, painful disease. Qurs-e-Mafasil, a herbal Unani preparation, is regarded as a potent treatment for Waja'al-Mafasil, a condition clinically similar to rheumatoid arthritis, but scientific evidence is scarce. Aim of the studyThis study aimed to assess the non-inferiority of Qurs-e-Mafasil compared to celecoxib in the treatment of patients with rheumatoid arthritis. Materials and methodsThis randomized controlled trial was conducted on seventy patients diagnosed with rheumatoid arthritis between the ages of 35 and 55 years. The participants were randomly allocated in a ratio of 3:2, with 42 participants in the test group and 28 participants in the control group. The test group was administered 2 tablets (each having 500 mg) of Qurs-e-Mafasil, while the control group was administered 1 capsule of Celecoxib 100 mg. Both medications were delivered for four weeks. The primary outcome measure was European League Against Rheumatism (EULAR) response criteria based on Disease Activity Score-28 (DAS28) assessed before and after therapy, whereas the secondary outcome measure was the change in joint pain severity as determined by a 100 mm Visual Analog Scale (VAS) at baseline and each follow-up. The safety of the interventions was evaluated based on adverse event monitoring at each follow-up and laboratory tests including hemogram, Liver Function Tests (LFTs), Kidney Function Tests (KFTs), and a complete urine examination performed at baseline and after four weeks of treatment. ResultsThe per-protocol analysis was done on 50 participants (30 in test group and 20 in control group) who completed the study duration. Thus, at the conclusion of the trial, participants in the test and control groups had either a moderate or no response based on EULAR response criteria. The odds ratio for no response versus moderate response between the test and the control groups was 0.71 (95% CI: 0.20–2.55) with p = 0.744. Moreover, the observed mean differences in VAS scores between the test and the control groups at 1st, 2nd, 3rd, and final follow-up were −0.33 (95% CI: −6.65 to 5.99, p = 0.916), 0.50 (95% CI: −5.63 to 6.63, p = 0.870), 2.42 (95% CI: −2.95 to 7.78, p = 0.370), and 3.00 (95% CI: −1.82 to 7.84, p = 0.219), respectively. ConclusionsThe differences in primary and secondary outcomes between the two groups indicate that Qurs-e-Mafāsil, a herbal Unani formulation containing Zingiber officinale Roscoe rhizome, Colchicum luteum Baker root, Piper nigrum L. fruit, and Withania somnifera (L.) Dunal. root, is comparable to celecoxib in the treatment of rheumatoid arthritis.

Molecular mechanism of Xiaohuoluo wan for rheumatoid arthritis by integrating in vitro and in vivo chemomics and network pharmacology.

The cause of rheumatoid arthritis (RA) is unclear. Xiaohuoluo wan (XHLW) is a classical Chinese medicine that is particularly effective in the treatment of RA. Given the chemical composition of XHLW at the overall level has been little studied and the molecular mechanism for the treatment of RA is not clear, we searched for the potential active compounds of XHLW and explored their anti-inflammatory mechanism in the treatment of RA by flexibly integrating the high-resolution ultra-performance liquid chromatography-mass spectrometry (UPLC-MS)-based in vitro and in vivo chemomics, network pharmacology, and other means. The results of the study identified that the active compounds of XHLW, such as alkaloids, nucleosides, and fatty acids, may play an anti-inflammatory role by regulating key targets such as IL-2, STAT1, JAK3, and MAPK8, inducing immune response through IL-17 signaling pathway, T-cell receptor, FoxO, tumor necrosis factor (TNF), and so forth, inhibiting the release of inflammatory factors and resisting oxidative stress and other pathways to treat RA. The results of this study provide referable data for the screening of active compounds and the exploration of molecular mechanisms of XHLW in the treatment of RA.

Role of Gut Microbiota in the Development and Management of Rheumatoid Arthritis: A Narrative Review.

Rheumatoid arthritis is an autoimmune condition that damages and inflames the joints. It causes severe disability and lowers the quality of life. While the precise cause of rheumatoid arthritis is still unknown, mounting evidence suggests that the gut microbiota, a diverse colony of bacteria that inhabits the gastrointestinal tract, may play a vital role in the progression and management of this debilitating condition. By evaluating relationships, probable processes, and therapeutic ramifications, this narrative review intends to examine the complex relationship between intestinal microbiota and rheumatoid arthritis.Additionally, for the management of rheumatoid arthritis, the review will assess prospective therapeutic approaches that target the gut flora. Multiple studies have shown that people with rheumatoid arthritis have dysbiosis or an imbalance in their gut microbial ecosystems. Increased intestinal permeability has been linked to changes in the gut microbiota, which allows the transfer of bacterial products into the bloodstream.Asearch was undertaken through PubMed in June 2023 using keywords like "microbiota", "rheumatoid arthritis" and "treatment". Overall 42 articles were included. Probiotics, prebiotics, and dietary changes are some examples of therapies that can be used to modify the gut microbiota and lessen symptoms, slower the progression of the disease, and enhance therapy results. Understanding the interplay between intestinal microbiota and rheumatoid arthritis will pave the way for innovative and personalized therapeutic interventions that could revolutionize the management of this chronic autoimmune disease.

Circulating interleukin-39 as a potential biomarker for rheumatoid arthritis diagnosis

BackgroundImbalances in cytokine networks have been shown to be a possible cause of rheumatoid arthritis (RA). The interleukin (IL)-12 family is involved in the pathogenesis of autoimmune diseases including RA, while IL-39 is a newly discovered member of the IL-12 family, although its role in RA remains unclear. The purpose of the present study was to detect the expression of IL-39 in the sera of patients with RA and its relationship with RA activity. MethodsWe recruited 46 patients with RA and 35 healthy controls at Ningbo Sixth Hospital. Blood samples were collected for biochemical analysis, and disease activity scores of 28 joints based on C-reactive protein were monitored. Serum concentrations of IL-39 were determined using an enzyme-linked immunosorbent assay. The Pearson correlation test was used to analyze the association between serum IL-39 levels and clinical indicators. ResultsSerum levels of IL-39 were significantly higher in patients with RA compared with healthy controls (p < 0.0001). IL-39 levels positively correlated with rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), and IgM; RF positively correlated with ESR. Receiver operating characteristic curve analysis showed that IL-39 has diagnostic value for RA (p < 0.0001). ConclusionsThe significant increase of IL-39 levels in serum of patients with RA and its positive correlation with clinical indicators suggest that IL-39 may serve as biomarker for the diagnosis of RA.

Association of mycoplasma pneumoniae and (rs9271366) HLA-DRB1gene polymorphism with the immune susceptibility to rheumatoid arthritis

Abstract Background: Rheumatoid arthritis (RA) is a chronic, inflammatory disease that affects the immune system. The primary cause of RA is unknown, but there is evidence that genetic and environmental factors also contribute to the development of the disease. Objectives: This study aimed to illustrate the relationship between the RA and Mycoplasma pneumoniae. Materials and Methods: The work was performed on 50 RA patients of various ages, ranging from 25 to 75 years of age, who were treated at the rheumatology clinic of the city of Medical Marjan between February 2022 to October 2022.Blood samples were used for DNA extraction. HLA-DRB1, IL-6 and mycoplasma were detected by enzyme-linked immunosorbent assay (ELISA). Results: The results showed that compared with RA patients not infected with Mycoplasma pneumoniae and healthy subjects, serum IL-6 concentration was significantly increased in RA patients infected with Mycoplasma pneumoniae. The results showed that serum concentrations of HLADRB1 were significantly elevated in RA patients infected with M. pneumoniae compared with RA patients not infected with M. pneumoniae and healthy subjects. Conclusions: In HLA-DRB1 the SNP rs9271366 was significantly associated with RA and G allele represent as dominant pathogenic allele in which the individual that carry GG and AG genotype have more susceptibility to mycoplasma infection than subjects that carry AA genotype (P = 0.036).

Interrelated grid of non-coding RNA: An important aspect in Rheumatoid Arthritis pathogenesis.

Inflammation and autoimmunity are the root cause of rheumatoid arthritis, a destructive disease of joints. Multiple biomolecules are involved in the pathogenesis of RA and are related to various events of molecular biology. RNA is a versatile biomolecule, playing numerous roles at structural, functional, and regulatory stages to maintain cellular homeostasis. The involvement of RNA (coding/non-coding) in disease development and progression has left a wide whole to fill with newer approaches. Non-coding RNAs belong to the housekeeping and regulatory categories and both have their specific roles, and their alteration causes specific implications in disease pathogenesis. Housekeeping RNAs, rRNA, tRNA and regulatory RNA, micro-RNA, circular RNA, piRNA and long non-coding RNA were found to be important regulators of inflammation. They work at the pre-and post-transcriptional levels and were found to be more intriguing to study their regulatory impact on disease pathogenesis. The review addresses a question on how the non-coding RNA gets involved in early RA pathogenesis and can be utilized to know their targets to understand the disease better and make way towards the unresolved mystery of RA development.

PROBIOTICS AS A MECHANISM TO REDUCE INFLAMMATION AND SLOW THE PROGRESSION OF RHEUMATOID ARTHRITIS

Introductions. Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and damage to joints, leading to pain and disability. Although the exact cause of RA is unknown, a dysregulated immune response and chronic inflammation are believed to play a key role in the development and progression of the disease. Recently, there has been increasing interest in the potential of probiotics as a therapeutic intervention for RA. Probiotics are live microorganisms that, when consumed in adequate amounts, confer health benefits on the host. In particular, several studies have suggested that probiotics may be able to modulate the immune system and reduce inflammation, potentially slowing the progression of RA.

Role of Sirtuins in the Pathogenesis of Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is an autoimmune and inflammatory disease leading to joint destruction. The causes of RA are not fully known. Most likely, the development of the disease depends on the coexistence of many factors, such as hereditary factors, immune system defects, gender, infectious agents, nicotine, and stress. Various epigenetic changes have been identified and correlated with the aggressive phenotype of RA, including the involvement of sirtuins, which are enzymes found in all living organisms. Their high content in the human body can slow down the aging processes, reduce cell death, counteract the appearance of inflammation, and regulate metabolic processes. Sirtuins can participate in several steps of RA pathogenesis. This narrative review presents, collects, and discusses the role of all sirtuins (1-7) in the pathogenesis of rheumatoid arthritis.

From vaccines to nanovaccines: A promising strategy to revolutionize rheumatoid arthritis treatment.

Rheumatoid arthritis (RA) is a joint-related autoimmune disease that is difficult to cure. Most therapeutics act to alleviate the symptoms but not correct the causes of RA. Novel strategies that specifically target the causes are highly needed for RA management. Currently, early interruption of RA is increasingly suggested but the corresponding therapeutics are not available. Vaccines that have shown great success to combat infection, cancer, degenerative diseases, autoimmune diseases, etc. are ideal candidates for a new generation of anti-RA therapeutics to correct the causes and prevent RA or interrupt RA in early phases. Anti-RA vaccines can be divided into two major categories. One is to induce neutralizing antibodies and the other is to induce antigen-specific immune tolerance. The vaccines are inherently linked to nanotechnology because they usually need a biomacromolecule or carrier to provoke sufficient immune responses. In the past decade, designed nanocarriers such as nanoparticles, liposomes, nanoemulsion, etc., have been applied to optimize the vaccines for autoimmune disease treatment. Nanotechnology endows vaccines with a higher biostability, tunable in vivo behavior, better targeting, co-delivery with stimulatory agents, regulatory effects on immune responses, etc. In this review, unmet medical needs for RA treatment and anti-RA vaccinology are first introduced. The development of anti-RA therapies from vaccines to nanovaccines are then reviewed and perspectives on how nanotechnology promotes vaccine development and advancement are finally provided. In addition, challenges for anti-RA vaccine development are summarized and advantages of nanovaccines are analyzed. In conclusion, nanovaccines will be a promising strategy to revolutionize the treatment of RA by correcting the causes in an early phase of RA.

Peficitinib inhibits fibroblast-like synoviocyte activation and angiogenic vascular endothelial tube formation via inhibitory effects on PDGF and VEGF signaling in addition to JAK

PurposePeficitinib and tofacitinib are known to suppress inflammation in rheumatoid arthritis (RA) by inhibiting Janus kinases (JAKs). However, these effects on tyrosine kinases other than JAKs have not yet been well investigated. We evaluated the effects of peficitinib and tofacitinib on platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptor tyrosine kinases (RTKs) and on the activation of fibroblast-like synoviocytes (FLSs) and endothelial cells, main pathological causes of RA. MethodsPeficitinib and tofacitinib were tested in PDGF and VEGF RTK assays. We then used FLSs derived from RA patient (RA-FLSs) and human umbilical vein endothelial cells (HUVECs) to study the effects of peficitinib and tofacitinib on PDGF- and VEGF-induced signal transduction and on the activation of RA-FLSs and endothelial cell tube formation. FindingsPeficitinib, not tofacitinib, inhibited both PDGF and VEGF RTKs in addition to JAKs in cell-free assay system. Peficitinib and tofacitinib attenuated PDGF- and VEGF-induced intracellular signal transduction pathways in RA-FLSs and HUVECs to varying degrees. Only peficitinib potently inhibited PDGF-induced secretion of interleukin-6, VEGF, and matrix metalloproteinase-3 in RA-FLSs, and endothelial cell tube formation by HUVECs. ConclusionPeficitinib may improve RA through inhibition of PDGF and VEGF signal transduction, in addition to JAK inhibition.

NIR-PTT/ROS-Scavenging/Oxygen-Enriched Synergetic Therapy for Rheumatoid Arthritis by a pH-Responsive Hybrid CeO2-ZIF-8 Coated with Polydopamine.

Rheumatoid arthritis (RA) is an inflammatory type of arthritis that causes joint pain and damage. The inflammatory cell infiltration (e.g., M1 macrophages), the poor O2 supply at the joint, and the excess reactive oxygen species (ROS)-induced oxidative injury are the main causes of RA. We herein report a polydopamine (PDA)-coated CeO2-dopped zeolitic imidazolate framework-8 (ZIF-8) nanocomposite CeO2-ZIF-8@PDA (denoted as CZP) that can synergistically treat RA. Under near-infrared (NIR) light irradiation, PDA efficiently scavenges ROS and results in an increased temperature in the inflamed area because of its good light-to-heat conversion efficiency. The rise of temperature serves to obliterate hyper-proliferative inflammatory cells accumulated in the diseased area while vastly promoting the collapse of the acidic-responsive skeleton of ZIF-8 to release the encapsulated CeO2. The released CeO2 exerts its catalase-like activity to relieve hypoxia by generating oxygen via the decomposition of H2O2 highly expressed in the inflammatory sites. Thus, the constructed CZP composite can treat RA through NIR-photothermal/ROS-scavenging/oxygen-enriched combinative therapy and show good regression of pro-inflammatory cytokines and hypoxia-inducible factor-1α (HIF-1α) in vitro and promising therapeutic effect on RA in rat models. The multimodal nano-platform reported herein is expected to shed light on the design of synergistic therapeutic nanomedicine for effective RA therapy.

MicroRNAs (miRNAs) in Cardiovascular Complications of Rheumatoid Arthritis (RA): What Is New?

Rheumatoid Arthritis (RA) is among the most prevalent and impactful rheumatologic chronic autoimmune diseases (AIDs) worldwide. Within a framework that recognizes both immunological activation and inflammatory pathways, the exact cause of RA remains unclear. It seems however, that RA is initiated by a combination between genetic susceptibility, and environmental triggers, which result in an auto-perpetuating process. The subsequently, systemic inflammation associated with RA is linked with a variety of extra-articular comorbidities, including cardiovascular disease (CVD), resulting in increased mortality and morbidity. Hitherto, vast evidence demonstrated the key role of non-coding RNAs such as microRNAs (miRNAs) in RA, and in RA-CVD related complications. In this descriptive review, we aim to highlight the specific role of miRNAs in autoimmune processes, explicitly on their regulatory roles in the pathogenesis of RA, and its CV consequences, their main role as novel biomarkers, and their possible role as therapeutic targets.

Correlation Between miR-223 Expression and Rheumatoid Arthritis

Patients diagnosed with rheumatoid arthritis (RA) show symptoms of joint affiliations. Focusing on the epigenetic factors leading to RA, the expression of several miRNAs are assumed to be one of the components influencing the cause of RA. Consequently, the increased expression of miR-223 is hypothesized to be involved in the pathogenesis of RA. This study aims to analyze the increased expression of miR-223 of RA patients in comparison with the normal and healthy representatives. Five methods from five different studies were involved in this review. The RNA was first isolated from heparinized venous blood or peripheral blood of RA patients and healthy controls. Reverse transcription was done to convert isolated RNA into cDNA and the expression of miR-223 was then measured using real-time PCR. The expression of miR-223 had exhibited a considerable increase in its concentration on RA patients when compared to healthy controls. Besides, the heightened concentration is taken upon consideration as miR-223 has a role in the regulation of the immune system and inflammatory responses.