nuclear transcription factor
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2021 ◽  
Vol 7 (50) ◽  
Author(s):  
Dan Cheng ◽  
Kevin Semmens ◽  
Elizabeth McManus ◽  
Qingrong Chen ◽  
Daoud Meerzaman ◽  
...  

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jordana Kron ◽  
Thomas Crawford ◽  
Virginia Mihalick ◽  
Frank Bogun ◽  
Jennifer H. Jordan ◽  
...  

Abstract Background Sarcoidosis is an inflammatory disease characterized by the formation of granulomas, which involve the heart in up to 25% of patients. Cardiac sarcoidosis can lead to life threatening arrhythmias and heart failure. While corticosteroids have been used as a treatment for over 50 years, they are associated with hypertension, diabetes, and weight gain, further increasing cardiovascular risk. Interleukin-1 (IL-1) is the prototypical proinflammatory cytokine that works to activate the nuclear transcription factor NF-kB, one of the targets of glucocorticoids. IL-1 also plays an important role also in the pathophysiology of heart disease including atherosclerosis, myocardial infarction, and myocarditis. Methods Building on a network of research collaborators developed in the Cardiac Sarcoidosis Consortium, we will investigate the feasibility and tolerability of treatment of CS with anakinra at two National Institute of Health Clinical and Translational Science Award (CTSA) hubs with expertise in cardiac sarcoidosis. In this pilot study, up to 28 patients with cardiac sarcoidosis will be recruited to compare the administration of an IL-1 blocker, anakinra, 100 mg daily on top of standard of care versus standard of care only for 28 days and followed for 180 days. Utilizing surrogate endpoints of changes in systemic inflammatory biomarkers and cardiac imaging, we aim to determine whether IL-1 blockade with anakinra can combat systemic and cardiac inflammation in patients with cardiac sarcoidosis. Discussion The current trial demonstrates an innovative collaborative approach to clinical trial development in a rare, understudied disease that disproportionately affects females and minorities. Trial Registration The trial was registered prospectively with ClinicalTrials.gov on July 12, 2019, identifier NCT04017936.


2021 ◽  
Vol 12 ◽  
Author(s):  
Hansen Yang ◽  
Jia Wang ◽  
Zheng Zhang ◽  
Rui Peng ◽  
Dan Lv ◽  
...  

Diabetic nephropathy (DN) is a serious complication of diabetes mellitus. Long non-coding RNAs (lncRNAs) are regulators in DN progression. However, the regulatory mechanisms of multiple lncRNAs in DN remain to be determined. Our aim was to investigate the function and molecular mechanism of lncRNA RNA component of mitochondrial RNAase P (Rmrp) in DN. Here, we observed that the expression of Rmrp was up-regulated in the kidney of db/db DN mice and high glucose induced glomerular mesangial cells (MC). More importantly, the abnormal transcription of Rmrp was induced by nuclear transcription factor Sp1, which promotes the proliferation and production of fibrotic markers in MC. Subsequently, we screened the miRNAs related to Rmrp and found that Rmrp and miR-1a-3p are co-localized at the subcellular level of MC, and Rmrp could directly binds to miR-1a-3p. Further mechanism research demonstrated that the elevated miR-1a-3p significantly attenuated the proliferation and fibrosis-promoting effects induced by up-regulation of Rmrp. At the same time, we also investigated that miR-1a-3p can directly bind to Jun D proto-oncogene (JunD), thereby regulating the protein level of JunD. Rmrp-induced proliferation and fibrogenesis were reversed by co-transfection with JunD siRNA. In summary, Sp1 induced lncRNA Rmrp could drive the expression of JunD via sponging miR-1a-3p in DN progression.


2021 ◽  
Vol 17 (2) ◽  
pp. 6-13
Author(s):  
M.V. Bondar ◽  
M.M. Pylypenko ◽  
O.A. Loskutov

This review describes in detail one of the key links in the pathogenesis of COVID-19 — the overproduction of pro-inflammatory cytokines that play a key role in the formation of acute respiratory distress syndrome, disseminated intravascular coagulation, multiple organ dysfunction syndromes, and causes high mortality among patients infected with COVID-19. The article deals with the basic directions of intensive therapy for the prevention of development as well as the treatment of cytokine storm and drugs for anti-cytokine therapy. Among drugs with anti-cytokine and anti-inflammatory properties, corticosteroids have the highest evidence base for efficacy and safety. The most promising drugs that require further clinical studies are those that inhibit the activity of the main intracellular regulator of the production of proinflammatory cytokines, the nuclear transcription factor kappa B of immunocompetent cells. These include turmeric-based preparations, which are now at the final stages of the pre-registration studies.


Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 112
Author(s):  
Wenli Luo ◽  
Li Li ◽  
Weina Xu ◽  
Jing Zhang ◽  
Jianxiong Xu

The cytotoxicity of docosahexaenoic acid (DHA) on normal cells is still unclear. This study investigated the effects of DHA on the cytotoxicity and possible mechanism in the BRL-3A cell. The cultured rat liver BRL-3A cell line was treated with 50, 100 and 200 μM DHA for 24 h. The cell viability was increased in the 50 and 100 μM DHA treatments, but decreased in the 200 μM DHA treatment. The 50, 100 and 200 μM DHA treatments increased the proportion of the apoptotic cells, the levels of lactate dehydrogenase (LDH), alkaline phosphatase (AKP) and IL-6 in the supernatant, and the ratio of the phosphonated p38MAPK to the p38MAPK (p-p38/p38) protein in the cells. The expression of TGF beta-activated kinase 1 (TAK1), nuclear transcription factor-κB p65 (NF-κB p65) and the inhibitor of NF-κB alpha (IκBα) mRNA, and the ratio of the phosphonated IκBα (p-IκBα) to IκBα protein were increased in the 200 μM DHA treatment, while the ratio of phosphonated extracellular regulated protein kinases (p-ERK) to ERK protein was decreased in the 200 μM DHA treatment. These results indicate that DHA-treated (50, 100 and 200 μM) BRL-3A cells for 24 h promotes cell apoptosis and inflammatory response, and the p38 MAPK, ERK and NF-κB signal pathways were involved in mediating the apoptosis and inflammatory response.


2021 ◽  
Vol 13 ◽  
Author(s):  
Teresa R. Kee ◽  
Pamela Espinoza Gonzalez ◽  
Jessica L. Wehinger ◽  
Mohammed Zaheen Bukhari ◽  
Aizara Ermekbaeva ◽  
...  

Rare mutations in the mitochondrial protein coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2) are associated with Parkinson’s disease (PD) and other Lewy body disorders. CHCHD2 is a bi-organellar mediator of oxidative phosphorylation, playing crucial roles in regulating electron flow in the mitochondrial electron transport chain and acting as a nuclear transcription factor for a cytochrome c oxidase subunit (COX4I2) and itself in response to hypoxic stress. CHCHD2 also regulates cell migration and differentiation, mitochondrial cristae structure, and apoptosis. In this review, we summarize the known disease-associated mutations of CHCHD2 in Asian and Caucasian populations, the physiological functions of CHCHD2, how CHCHD2 mutations contribute to α-synuclein pathology, and current animal models of CHCHD2. Further, we discuss the necessity of continued investigation into the divergent functions of CHCHD2 and CHCHD10 to determine how mutations in these similar mitochondrial proteins contribute to different neurodegenerative diseases.


2021 ◽  
Vol 5 (3) ◽  
pp. 1-5
Author(s):  
Olga S. León Fernández ◽  
Gabriel Takon Oru ◽  
Renate Viebhan Hansler ◽  
Gilberto López Cabreja ◽  
Irainis Serrano Espinosa ◽  
...  

Introduction: Medical ozone has been used with safety and efficacy in different diseases of oxidative etiology, for the most part involving autoimmune diseases. Methods: An analysis of the pharmacological mechanism of action of ozone was carried out to explain its clinical effectiveness and its positive response in clinical patients to COVID-19. This was done in the context of the different therapeutic targets that have been demonstrated for ozone in other diseases (autoimmune and hypoxia status). Results: Based on the intestine/lung functional axis, the necessity of rectal insufflation as route of application with the aim of attaining improved results using medical ozone against COVID 19 is demonstrated. It was possible to identify at least nine adverse events/molecules which were targets of regulation through medical ozone in other diseases, including innate immune response, nuclear transcription factor NF-kB, “cytokine storm”, inflammation, severe acute respiratory syndrome and coagulopathy. Some of them lead to multi organ failure. Finally, a brief analysis is undertaken to show the regulatory effects of ozone versus the comorbidities contributing to virus lethality, including hyperglycemia and its vascular complications. Conclusions: Medical ozone is effective against COVID-19/SARS-CoV-2: due to the multiple targets it is able to regulate and thereby achieve a positive patient response.


2020 ◽  
Author(s):  
Ludmila F M F Cardozo ◽  
Livia A Alvarenga ◽  
Marcia Ribeiro ◽  
Lu Dai ◽  
Paul G Shiels ◽  
...  

Abstract Sulforaphane (SFN) is a sulfur-containing isothiocyanate found in cruciferous vegetables (Brassicaceae) and a well-known activator of nuclear factor-erythroid 2-related factor 2 (Nrf2), considered a master regulator of cellular antioxidant responses. Patients with chronic diseases, such as diabetes, cardiovascular disease, cancer, and chronic kidney disease (CKD) present with high levels of oxidative stress and a massive inflammatory burden associated with diminished Nrf2 and elevated nuclear transcription factor-κB-κB expression. Because it is a common constituent of dietary vegetables, the salutogenic properties of sulforaphane, especially it’s antioxidative and anti-inflammatory properties, have been explored as a nutritional intervention in a range of diseases of ageing, though data on CKD remain scarce. In this brief review, the effects of SFN as a senotherapeutic agent are described and a rationale is provided for studies that aim to explore the potential benefits of SFN-rich foods in patients with CKD.


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