Bortezomib followed by autologous stem cell transplantation in a patient with rheumatoid arthritis

Liu, Junru; Li, Juan; Chen, Meilan; Kuang, Lifen

doi:10.1097/md.0000000000005760

Cited by 8 publications

(4 citation statements)

References 20 publications

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“…We and others have shown that BZ, at very low nontumor-suppressive doses, can modulate immune cell activation (28,29). Recent clinical studies demonstrated that BZ is an effective immunomodulatory therapy for arthritis, transplant rejection, graft-versus-host disease, and autoimmune diseases (30)(31)(32)(33)(34). BZ appears to be a safe immunomodulatory drug with a very favorable side effect profile (35).…”

Section: Genetic Damping Of Myeloid Activation Ameliorates Iso-induce...mentioning

confidence: 99%

Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy

Liao¹,

Chang²,

Tang³

et al. 2022

JCI Insight

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Takotsubo syndrome (TTS) is an acute, stress-induced cardiomyopathy that occurs predominantly in women after extreme physical and/or emotional stress. To date, our understanding of the molecular basis for TTS remains unknown and, consequently, specific therapies are lacking. Myocardial infiltration of monocytes and macrophages in TTS has been documented in clinical studies. However, the functional importance of these findings remains poorly understood. Here, we show that a single high dose of isoproterenol (ISO) in mice induced a TTS-like cardiomyopathy phenotype characterized by female predominance, severe cardiac dysfunction, and robust myocardial infiltration of macrophages. Single-cell RNA-Seq studies of myocardial immune cells revealed that TTS-like cardiomyopathy is associated with complex activation of innate and adaptive immune cells in the heart, and macrophages were identified as the dominant immune cells. Global macrophage depletion (via clodronate liposome administration) or blockade of macrophage infiltration (via a CCR2 antagonist or in CCR2-KO mice) resulted in recovery of cardiac dysfunction in ISO-challenged mice. In addition, damping myeloid cell activation by HIF1α deficiency or exposure to the immunomodulatory agent bortezomib ameliorated ISO-induced cardiac dysfunction. Collectively, our findings identify macrophages as a critical regulator of TTS pathogenesis that can be targeted for therapeutic gain.

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Section: Genetic Damping Of Myeloid Activation Ameliorates Iso-induce...mentioning

confidence: 99%

Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy

Liao¹,

Chang²,

Tang³

et al. 2022

JCI Insight

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“…However, bortezomib also significantly improved general symptoms in pSS patients, particularly fatigue, reduced serum globulin levels, and serum viscosity, according to previous reports [ 47 ]. In both animal experiments and clinical trials, bortezomib ameliorated symptoms after the first cycle and continued to improve gradually in patients with refractory RA [ 48 ]. In addition, we also predicted protease inhibitors, such as carfilzomib, oprozomib, and marizomib, as candidate drugs for the treatment of RA and pSS.…”

Section: Discussionmentioning

confidence: 99%

Potential mechanisms and drug prediction of Rheumatoid Arthritis and primary Sjögren’s Syndrome: A public databases-based study

Wu,

Wang,

Gao

et al. 2024

PLoS ONE

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Rheumatoid arthritis (RA) and primary Sjögren’s syndrome (pSS) are the most common systemic autoimmune diseases, and they are increasingly being recognized as occurring in the same patient population. These two diseases share several clinical features and laboratory parameters, but the exact mechanism of their co-pathogenesis remains unclear. The intention of this study was to investigate the common molecular mechanisms involved in RA and pSS using integrated bioinformatic analysis. RNA-seq data for RA and pSS were picked up from the Gene Expression Omnibus (GEO) database. Co-expression genes linked with RA and pSS were recognized using weighted gene co-expression network analysis (WGCNA) and differentially expressed gene (DEG) analysis. Then, we screened two public disease–gene interaction databases (GeneCards and Comparative Toxicogenomics Database) for common targets associated with RA and pSS. The DGIdb database was used to predict therapeutic drugs for RA and pSS. The Human microRNA Disease Database (HMDD) was used to screen out the common microRNAs associated with RA and pSS. Finally, a common miRNA–gene network was created using Cytoscape. Four hub genes (CXCL10, GZMA, ITGA4, and PSMB9) were obtained from the intersection of common genes from WGCNA, differential gene analysis and public databases. Twenty-four drugs corresponding to hub gene targets were predicted in the DGIdb database. Among the 24 drugs, five drugs had already been reported for the treatment of RA and pSS. Other drugs, such as bortezomib, carfilzomib, oprozomib, cyclosporine and zidovudine, may be ideal drugs for the future treatment of RA patients with pSS. According to the miRNA–gene network, hsa-mir-21 may play a significant role in the mechanisms shared by RA and pSS. In conclusion, we identified commom targets as potential biomarkers in RA and pSS from publicly available databases and predicted potential drugs based on the targets. A new understanding of the molecular mechanisms associated with RA and pSS is provided according to the miRNA–gene network.

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“…In a recent study, delanzomib, a novel proteasome inhibitor, was successfully used together with adalimumab in a rat model of rheumatoid arthritis [ 147 ]. Moreover, two case reports showed remission of rheumatoid arthritis complicated with multiple myeloma [ 148 ] or TEMPI syndrome [ 149 ] after administration of bortezomib.…”

Section: Discussionmentioning

confidence: 99%

Gene Ontology Analysis Highlights Biological Processes Influencing Non-Response to Anti-TNF Therapy in Rheumatoid Arthritis

2022

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Anti-TNF therapy has significantly improved disease control in rheumatoid arthritis, but a fraction of rheumatoid arthritis patients do not respond to anti-TNF therapy or lose response over time. Moreover, the mechanisms underlying non-response to anti-TNF therapy remain largely unknown. To date, many single biomarkers of response to anti-TNF therapy have been published but they have not yet been analyzed as a system of interacting nodes. The aim of our study is to systematically elucidate the biological processes underlying non-response to anti-TNF therapy in rheumatoid arthritis using the gene ontologies of previously published predictive biomarkers. Gene networks were constructed based on published biomarkers and then enriched gene ontology terms were elucidated in subgroups using gene ontology software tools. Our results highlight the novel role of proteasome-mediated protein catabolic processes (p = 2.91 × 10−15) and plasma lipoproteins (p = 4.55 × 10−11) in anti-TNF therapy response. The results of our gene ontology analysis help elucidate the biological processes underlying non-response to anti-TNF therapy in rheumatoid arthritis and encourage further study of the highlighted processes.

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Bortezomib followed by autologous stem cell transplantation in a patient with rheumatoid arthritis

Cited by 8 publications

References 20 publications

Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy

Cardiac macrophages regulate isoproterenol-induced Takotsubo-like cardiomyopathy

Potential mechanisms and drug prediction of Rheumatoid Arthritis and primary Sjögren’s Syndrome: A public databases-based study

Gene Ontology Analysis Highlights Biological Processes Influencing Non-Response to Anti-TNF Therapy in Rheumatoid Arthritis

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