scholarly journals Emerging role of interleukin-1 in cardiovascular diseases

2009 ◽  
pp. 481-498
Author(s):  
B Vicenová ◽  
V Vopálenský ◽  
L Burýšek ◽  
M Pospíšek

There is an increasing evidence linking dysbalance between various proinflammatory mediators and higher risk of cardiovascular events and pathologies. Likewise, some of the cardiovascular diseases lately appeared to have an autoimmune component. Interleukin-1 (IL-1), a master regulator of diverse inflammatory processes in higher eukaryotes and the key player in numerous autoimmune disorders including rheumatoid arthritis, diabetes mellitus or systemic sclerosis, has recently been proved to be involved in development of several cardiovascular diseases as well. This report aims to give a summary on current knowledge about the IL-1 signaling pathways and about the implication of IL-1 and the IL-1 receptor antagonist (IL-1Ra) in some of the diseases of the cardiovascular system.

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Samuel García ◽  
Carmen Conde

Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme with a crucial role in the maintenance of genomic stability. In addition to the role of PARP-1 in DNA repair, multiple studies have also demonstrated its involvement in several inflammatory diseases, such as septic shock, asthma, atherosclerosis, and stroke, as well as in cancer. In these diseases, the pharmacological inhibition of PARP-1 has shown a beneficial effect, suggesting that PARP-1 regulates their inflammatory processes. In recent years, we have studied the role of PARP-1 in rheumatoid arthritis, as have other researchers, and the results have shown that PARP-1 has an important function in the development of this disease. This review summarizes current knowledge on the effects of PARP-1 in rheumatoid arthritis.


PPAR Research ◽  
2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Mini Chandra ◽  
Sumitra Miriyala ◽  
Manikandan Panchatcharam

Peroxisome proliferator-activated receptor Gamma (PPARγ), a ligand-activated transcription factor, has a role in various cellular functions as well as glucose homeostasis, lipid metabolism, and prevention of oxidative stress. The activators of PPARγare already widely used in the treatment of diabetes mellitus. The cardioprotective effect of PPARγactivation has been studied extensively over the years making them potential therapeutic targets in diseases associated with cardiovascular disorders. However, they are also associated with adverse cardiovascular events such as congestive heart failure and myocardial infarction. This review aims to discuss the role of PPARγin the various cardiovascular diseases and summarize the current knowledge on PPARγagonists from multiple clinical trials. Finally, we also review the new PPARγagonists under development as potential therapeutics with reduced or no adverse effects.


2021 ◽  
Vol 48 (3) ◽  
pp. 2843-2852
Author(s):  
S. Berardi ◽  
A. Corrado ◽  
N. Maruotti ◽  
D. Cici ◽  
F. P. Cantatore

AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.


2017 ◽  
Vol 13 (7) ◽  
pp. 486-498 ◽  
Author(s):  
L.K. Sokolova ◽  
V.M. Pushkarev ◽  
V.V. Pushkarev ◽  
O.I. Kovzun ◽  
M.D. Tronko

2013 ◽  
Vol 59 (8) ◽  
pp. 1166-1174 ◽  
Author(s):  
Fina Lovren ◽  
Subodh Verma

BACKGROUND Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation. CONTENT This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells. SUMMARY MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.


Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3155 ◽  
Author(s):  
Mrinalini Dey ◽  
Maurizio Cutolo ◽  
Elena Nikiphorou

Background: The role of nutrition in the pathogenesis of rheumatic diseases, including rheumatoid arthritis (RA), has gained increasing attention in recent years. A growing number of studies have focussed on the diverse nutritional contents of beverages, and their possible role in the development and progression of RA. Main body: We aimed to summarise the current knowledge on the role of a range of beverages in the context of RA. Beverages have a key role within the mosaic of autoimmunity in RA and potential to alter the microbiome, leading to downstream effects on inflammatory pathways. The molecular contents of beverages, including coffee, tea, and wine, have similarly been found to interfere with immune signalling pathways, some beneficial for disease progression and others less so. Finally, we consider beverages in the context of wider dietary patterns, and how this growing body of evidence may be harnessed by the multidisciplinary team in patient management. Conclusions: While there is increasing work focussing on the role of beverages in RA, integration of discussions around diet and lifestyle in our management of patients remains sparse. Nutrition in RA remains a controversial topic, but future studies, especially on the role of beverages, are likely to shed further light on this in coming years.


BMJ Open ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. e032633 ◽  
Author(s):  
Kuo-Liong Chien ◽  
Ting-Yu Lin ◽  
Chen-Yang Hsu ◽  
Chang-Chuan Chan ◽  
Tony Hsiu-Hsi Chen ◽  
...  

ObjectivesThe role of faecal haemoglobin as a colorectal cancer screening tool has been demonstrated. However, the association between the faecal haemoglobin concentration and the risk of cardiovascular disease events and deaths is still unclear.DesignCohort study design.SettingPopulation-based organised integrated service screening in Keelung City, TaiwanParticipantsA total of 33 355 healthy individuals aged over 40 years who were free of cardiovascular disease at study entry were followed up.Main outcomes and measuresNewly diagnosed cardiovascular disease events and deaths.ResultsAfter a median follow-up of 2.39 years, a total of 2768 participants developed cardiovascular events, and after a median follow-up of 8.43 years, 317 cases of cardiovascular deaths occurred. The risk of cardiovascular disease increased with baseline faecal haemoglobin in a dose–response manner, yielding a significant elevated risk of cardiovascular disease in parallel with the incremental concentration of faecal haemoglobin (adjusted HRs=1.04, 1.10, 1.40 and 1.23 for faecal haemoglobin concentrations of 1–19, 20–49, 50–99 and ≥100 ng/mL, trend test, p<0.0001, as compared with the reference group with undetectable faecal haemoglobin concentrations). A similar pattern was observed for the risk of cardiovascular disease deaths. In addition, the faecal haemoglobin improved the prediction performance of the model for the risk of cardiovascular diseases; the integrated discrimination improvement was 0.3% (p<0.001) for cardiovascular events and 0.1% (p=0.020) for cardiovascular deaths.ConclusionsOur data support that faecal haemoglobin concentrations may be associated with the risk of cardiovascular diseases. The biological mechanisms underlying the role of faecal haemoglobin as health outcomes should be investigated.


2005 ◽  
Vol 108 (3) ◽  
pp. 205-213 ◽  
Author(s):  
Sieglinde KOFLER ◽  
Thomas NICKEL ◽  
Michael WEIS

Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1, IL-6 and IFN-γ (interferon-γ)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-β1 (transforming growth factor-β1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.


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