Iguratimod dose dependently inhibits the expression of citrullinated proteins and peptidylarginine deiminases 2 and 4 in neutrophils from rheumatoid arthritis patients

Li, Bingtong; Li, Ping; Bi, Liqi

doi:10.1007/s10067-019-04835-4

Cited by 10 publications

(10 citation statements)

References 41 publications

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“…Serum levels of inflammatory factors in NOD mice significantly decreased after administering different IGU doses, similar to the results obtained with IGU for RA and ankylosing spondylitis 28 , 29 . IGU can inhibit the IL-1β, TNF-α, IL-17, and IL-6 expressions.…”

Section: Discussionsupporting

confidence: 83%

Effects of iguratimod on inflammatory factors and apoptosis of submandibular gland epithelial cells in NOD mice

Wang,

Yu,

Yang

et al. 2023

Sci Rep

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Non-obese diabetic (NOD) mice were taken as primary Sjögren’s syndrome (pSS) model mice to examine the therapeutic impact of iguratimod (IGU) on inflammatory factors levels and apoptosis of submandibular epithelial cells, and provide experimental basis for the treatment of pSS by iguratimod. Twenty-four NOD murine models were divided into the model, high-dose (IGU 30 mg/kg) and low-dose (IGU 10 mg/kg) groups, eight mice per group. The normal control group comprised eight C57B/L mice. From 8 weeks of age, the NOD mice were administered IGU by intragastric gavage administration every day for 8 weeks; their water consumption, saliva secretion, submandibular gland, and spleen indices were measured. The levels of serum inflammatory factor (IL-1β, TNF-α, IL-6, and IL-17) were evaluated, and Bax, caspase-3, and Bcl-2 levels were detected. The histological alterations in the submandibular glands were discovered. IGU can reduce the water intake of NOD mice (p < 0.01), increase the saliva secretion and the submandibular gland index (p < 0.01); reduce the spleen index and the serum inflammatory factors (p < 0.01); improve the pathological tissue damage and cell apoptosis of the submandibular gland (p < 0.05). IGU can reduce the expression levels of inflammatory mediators in the serum and the extent of lymphocyte infiltration and apoptosis in submandibular gland epithelial cells. It can also regulate apoptosis-related protein expression, thereby improving the secretory function of exocrine glands.

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Section: Discussionsupporting

confidence: 83%

Effects of iguratimod on inflammatory factors and apoptosis of submandibular gland epithelial cells in NOD mice

Wang,

Yu,

Yang

et al. 2023

Sci Rep

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“…Iguratimod inhibits citrulline protein expression in neutrophils of patients with rheumatoid arthritis at an appropriate concentration, similar to MTX and dexamethasone; the inhibitory effect is mediated by the down-regulation of peptidylarginine deiminase, which provides insights into the mechanism of Iguratimod in the treatment of rheumatoid arthritis. This study can guide the treatment of rheumatoid arthritis and promote the identification of other therapeutic targets ( 59 ).…”

Section: Iguratimod: a Chemical Substance With Multiple Pharmacologic...mentioning

confidence: 99%

Research progress on the clinical application and mechanism of iguratimod in the treatment of autoimmune diseases and rheumatic diseases

Long,

Zeng,

et al. 2023

Front. Immunol.

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Autoimmune diseases are affected by complex pathophysiology involving multiple cell types, cytokines, antibodies and mimicking factors. Different drugs are used to improve these autoimmune responses, including nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, antibodies, and small molecule drugs (DMARDs), which are prevalent clinically in the treatment of rheumatoid arthritis (RA), etc. However, low cost-effectiveness, reduced efficacy, adverse effects, and patient non-response are unattractive factors driving the development of new drugs such as iguratimod. As a new disease-modifying antirheumatic drug, iguratimod has pharmacological activities such as regulating autoimmune disorders, inflammatory cytokines, regulating immune cell activation, differentiation and proliferation, improving bone metabolism, and inhibiting fibrosis. In recent years, clinical studies have found that iguratimod is effective in the treatment of RA, SLE, IGG4-RD, Sjogren ‘s syndrome, ankylosing spondylitis, interstitial lung disease, and other autoimmune diseases and rheumatic diseases. The amount of basic and clinical research on other autoimmune diseases is also increasing. Therefore, this review systematically reviews the latest relevant literature in recent years, reviews the research results in recent years, and summarizes the research progress of iguratimod in the treatment of related diseases. This review highlights the role of iguratimod in the protection of autoimmune and rheumatic bone and related immune diseases. It is believed that iguratimod’s unique mode of action and its favorable patient response compared to other DMARDs make it a suitable antirheumatic and bone protective agent in the future.

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“…Moreover, IGU also downregulates the neutrophil extracellular trap. 49 Immunotherapeutic treatments using therapeutic anticitrullinated protein autoantibodies (tACPAs) reduce the immunological burden caused by hyper-citrullinated proteins. These tACPAs target a specific epitope region in the N-terminal sequence of histone-2A.…”

Section: Peptidyl-arginine-deiminase (Pad)mentioning

confidence: 99%

Unveiling Novel Drug Targets and Emerging Therapies for Rheumatoid Arthritis: A Comprehensive Review

Khokhar,

Dey,

Tomo

et al. 2024

ACS Pharmacol. Transl. Sci.

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Rheumatoid arthritis (RA) is a chronic debilitating autoimmune disease, that causes joint damage, deformities, and decreased functionality. In addition, RA can also impact organs like the skin, lungs, eyes, and blood vessels. This autoimmune condition arises when the immune system erroneously targets the joint synovial membrane, resulting in synovitis, pannus formation, and cartilage damage. RA treatment is often holistic, integrating medication, physical therapy, and lifestyle modifications. Its main objective is to achieve remission or low disease activity by utilizing a “treat-to-target” approach that optimizes drug usage and dose adjustments based on clinical response and disease activity markers. The primary RA treatment uses disease-modifying antirheumatic drugs (DMARDs) that help to interrupt the inflammatory process. When there is an inadequate response, a combination of biologicals and DMARDs is recommended. Biological therapies target inflammatory pathways and have shown promising results in managing RA symptoms. Close monitoring for adverse effects and disease progression is critical to ensure optimal treatment outcomes. A deeper understanding of the pathways and mechanisms will allow new treatment strategies that minimize adverse effects and maintain quality of life. This review discusses the potential targets that can be used for designing and implementing precision medicine in RA treatment, spotlighting the latest breakthroughs in biologics, JAK inhibitors, IL-6 receptor antagonists, TNF blockers, and disease-modifying noncoding RNAs.

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Iguratimod dose dependently inhibits the expression of citrullinated proteins and peptidylarginine deiminases 2 and 4 in neutrophils from rheumatoid arthritis patients

Cited by 10 publications

References 41 publications

Effects of iguratimod on inflammatory factors and apoptosis of submandibular gland epithelial cells in NOD mice

Effects of iguratimod on inflammatory factors and apoptosis of submandibular gland epithelial cells in NOD mice

Research progress on the clinical application and mechanism of iguratimod in the treatment of autoimmune diseases and rheumatic diseases

Unveiling Novel Drug Targets and Emerging Therapies for Rheumatoid Arthritis: A Comprehensive Review

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