scholarly journals The critical role of epigenetic mechanism in PM2.5-induced cardiovascular diseases

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Qinglin Sun ◽  
Xiaoke Ren ◽  
Zhiwei Sun ◽  
Junchao Duan
Keyword(s):  
Cardiovascular Health ◽  
Human Life ◽  
Fine Particulate Matter ◽  
Critical Role ◽  
Underlying Mechanism ◽  
Epidemiological Studies ◽  
Epigenetic Mechanism ◽  
Epigenetic Changes ◽  
Functional Changes ◽  
Adults And Children

AbstractCardiovascular disease (CVD) has become the leading cause of death worldwide, which seriously threatens human life and health. Epidemiological studies have confirmed the occurrence and development of CVD are closely related to air pollution. In particular, fine particulate matter (PM2.5) is recognized as an important environmental factor contributing to increased morbidity, mortality and hospitalization rates among adults and children. However, the underlying mechanism by which PM2.5 promotes CVD development remains unclear. With the development of epigenetics, recent studies have shown that PM2.5 exposure may induce or aggravate CVD through epigenetic changes. In order to better understand the potential mechanisms, this paper reviews the epigenetic changes of CVD caused by PM2.5. We summarized the epigenetic mechanisms of PM2.5 causing cardiovascular pathological damage and functional changes, mainly involving DNA methylation, non-coding RNA, histone modification and chromosome remodeling. It will provide important clues for exploring the biological mechanisms affecting cardiovascular health.

scholarly journals The Emerging Role of Ten-Eleven Translocation 1 in Epigenetic Responses to Environmental Exposures

2020 ◽  
Vol 13 ◽  
pp. 251686572091015 ◽  
Author(s):  
Tao Zhu ◽  
Anthony P Brown ◽  
Hong Ji
Keyword(s):  
Therapeutic Potential ◽  
Critical Role ◽  
Environmental Exposures ◽  
Epidemiological Studies ◽  
Epigenetic Changes ◽  
Molecular Processes ◽  
Molecular Events ◽  
Negative Impacts ◽  
The Impact

Mounting evidence from epidemiological studies and animal models has linked exposures to environmental factors to changes in epigenetic markers, especially in DNA methylation. These epigenetic changes may lead to dysregulation of molecular processes and functions and mediate the impact of environmental exposures in complex diseases. However, detailed molecular events that result in epigenetic changes following exposures remain unclear. Here, we review the emerging evidence supporting a critical role of ten-eleven translocation 1 (TET1) in mediating these processes. Targeting TET1 and its associated pathways may have therapeutic potential in alleviating negative impacts of environmental exposures, preventing and treating exposure-related diseases.

scholarly journals n-6 Fatty acids and cardiovascular health: a review of the evidence for dietary intake recommendations

2010 ◽  
Vol 104 (6) ◽  
pp. 788-796 ◽  
Author(s):  
Sébastien Czernichow ◽  
Daniel Thomas ◽  
Eric Bruckert
Keyword(s):  
Dietary Intake ◽  
Cardiovascular Health ◽  
Critical Role ◽  
Epidemiological Studies ◽  
Protective Role ◽  
Cvd Risk ◽  
Pufa Intake ◽  
Cholesterol Levels ◽  
Excessive Consumption ◽  
Review Recommendation

n-6 PUFA are well known for their critical role in many physiological functions and seem to reduce risks of CHD. However, some argue that excessive consumption of n-6 PUFA may lead to adverse effects on health and therefore recommend reducing dietary n-6 PUFA intake or fixing an upper limit. In this context, the present work aimed to review evidence on the link between n-6 PUFA and risks of CVD. Epidemiological studies show that n-6 PUFA dietary intake significantly lowers blood LDL-cholesterol levels. In addition, n-6 PUFA intake does not increase several CVD risk factors such as blood pressure, inflammatory markers, haemostatic parameters and obesity. Data from prospective cohort and interventional studies converge towards a specific protective role of dietary n-6 PUFA intake, in particular linoleic acid, against CVD. n-6 PUFA benefits are even increased when SFA intake is also reduced. In regards to studies examined in this narrative review, recommendation for n-6 PUFA intake above 5 %, and ideally about 10 %, of total energy appears justified.

scholarly journals Influence of Benzo(a)pyrene on Different Epigenetic Processes

2021 ◽  
Vol 22 (24) ◽  
pp. 13453
Author(s):  
Bożena Bukowska ◽  
Paulina Sicińska
Keyword(s):  
Lung Cancer ◽  
Dna Methylation ◽  
Histone Deacetylases ◽  
Polyaromatic Hydrocarbons ◽  
Methylation Status ◽  
Underlying Mechanism ◽  
Epidemiological Studies ◽  
Dna Methyltransferases ◽  
Epigenetic Changes ◽  
Marine Medaka

Epigenetic changes constitute one of the processes that is involved in the mechanisms of carcinogenicity. They include dysregulation of DNA methylation processes, disruption of post-translational patterns of histone modifications, and changes in the composition and/or organization of chromatin. Benzo(a)pyrene (BaP) influences DNA methylation and, depending on its concentrations, as well as the type of cell, tissue and organism it causes hypomethylation or hypermethylation. Moreover, the exposure to polyaromatic hydrocarbons (PAHs), including BaP in tobacco smoke results in an altered methylation status of the offsprings. Researches have indicated a potential relationship between toxicity of BaP and deregulation of the biotin homeostasis pathway that plays an important role in the process of carcinogenesis. Animal studies have shown that parental-induced BaP toxicity can be passed on to the F1 generation as studied on marine medaka (Oryzias melastigma), and the underlying mechanism is likely related to a disturbance in the circadian rhythm. In addition, ancestral exposure of fish to BaP may cause intergenerational osteotoxicity in non-exposed F3 offsprings. Epidemiological studies of lung cancer have indicated that exposure to BaP is associated with changes in methylation levels at 15 CpG; therefore, changes in DNA methylation may be considered as potential mediators of BaP-induced lung cancer. The mechanism of epigenetic changes induced by BaP are mainly due to the formation of CpG-BPDE adducts, between metabolite of BaP—BPDE and CpG, which leads to changes in the level of 5-methylcytosine. BaP also acts through inhibition of DNA methyltransferases activity, as well as by increasing histone deacetylases HDACs, i.e., HDAC2 and HDAC3 activity. The aim of this review is to discuss the mechanism of the epigenetic action of BaP on the basis of the latest publications.

scholarly journals OTUB1 Promotes Progression and Proliferation of Prostate Cancer via Deubiquitinating and Stabling Cyclin E1

2021 ◽  
Vol 8 ◽  
Author(s):  
Yihao Liao ◽  
Ning Wu ◽  
Keke Wang ◽  
Miaomiao Wang ◽  
Youzhi Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Nude Mice ◽  
Critical Role ◽  
Underlying Mechanism ◽  
Clinical Prognosis ◽  
Functional Changes ◽  
Cyclin E1 ◽  
Tumor Tissues ◽  
And Migration

Background: Prostate cancer (PCa) is currently the most common cancer among males worldwide. It has been reported that OTUB1 plays a critical role in a variety of tumors and is strongly related to tumor proliferation, migration, and clinical prognosis. The aim of this research is to investigate the regulatory effect of OTUB1 on PCa proliferation and the underlying mechanism.Methods: Using the TCGA database, we identified that OTUB1 was up-regulated in PCa, and observed severe functional changes in PC3 and C4-2 cells through overexpression or knock down OTUB1. Heterotopic tumors were implanted subcutaneously in nude mice and IHC staining was performed on tumor tissues. The relationship between OTUB1 and cyclin E1 was identified via Western blotting and immunoprecipitations assays.Results: We found that the expression of OTUB1 in PCa was significantly higher than that in Benign Prostatic Hyperplasia (BPH). Overexpression OTUB1 obviously promoted the proliferation and migration of PC3 and C4-2 cells via mediating the deubiquitinated Cyclin E1, while OTUB1 knockout has the opposite effect. The nude mice experiment further explained the above conclusions. We finally determined that OTUB1 promotes the proliferation and progression of PCa via deubiquitinating and stabling Cyclin E1.Conclusions: Our findings reveal the critical role of OTUB1 in PCa, and OTUB1 promotes the proliferation and progression of PCa via deubiquitinating and stabilizing Cyclin E1. Blocking OTUB1/Cyclin E1 axis or applying RO-3306 could significantly repress the occurrence and development of PCa. OTUB1/Cyclin E1 axis might provide a new and potential therapeutic target for PCa.

scholarly journals To which extent are per-and poly-fluorinated substances associated to metabolic syndrome?

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Maryam Zare Jeddi ◽  
Rozita Soltanmohammadi ◽  
Giulia Barbieri ◽  
Aline S. C. Fabricio ◽  
Gisella Pitter ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
General Population ◽  
Meta Analysis ◽  
Small Body ◽  
Epidemiological Studies ◽  
Cross Sectional ◽  
Random Effects Models ◽  
Epidemiologic Evidence ◽  
Adults And Children ◽  
Meta Analyses

Abstract Exposure to per- and polyfluoroalkyl substances (PFAS), ubiquitous persistent environmental contaminants, has led to substantial global concern due to their potential environmental and human health effects. Several epidemiological studies have assessed the possible association between PFAS exposure and risk of metabolic syndrome (MetS), however, the results are ambiguous. The aim of this study was to assess the current human epidemiologic evidence on the association between exposure to PFAS and MetS. We performed a systematic search strategy using three electronic databases (PubMed, Scopus, and Web of Science) for relevant studies concerning the associations of PFAS with MetS and its clinical relevance from inception until January 2021. We undertook meta-analyses where there were five or more studies with exposure and outcomes assessments that were reasonably comparable. The pooled odd ratios (ORs) were calculated using random effects models and heterogeneity among studies was assessed by I2 index and Q test. A total of 12 cross-sectional studies (10 studies on the general population and two studies in the occupational settings) investigated the association between PFAS exposure and MetS. We pooled data from seven studies on the general population for perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) and five studies for perfluorohexanesulfonate (PFHxS) and perfluorononanoic acid (PFNA). Predominately, most studies reported no statistically significant association between concentrations of PFAS and MetS. In the meta-analysis, the overall measure of effect was not statistically significant, showing no evidence of an association between concentrations of PFOA, PFOS, PFNA, and PFHxS and the risk of MetS. Based on the results of the meta-analysis, current small body of evidence does not support association between PFAS and MetS. However, due to limited number of studies and substantial heterogeneity, results should be interpreted with caution. Further scrutinizing cohort studies are needed to evaluate the association between various and less well-known PFAS substances and their mixture with MetS and its components in both adults and children in different settings.

scholarly journals Specialized Pro-Resolving Lipid Mediators in Neonatal Cardiovascular Physiology and Diseases

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 933
Author(s):  
Andrea Gila-Diaz ◽  
Gloria Herranz Carrillo ◽  
Pratibha Singh ◽  
David Ramiro-Cortijo
Keyword(s):  
Tissue Repair ◽  
Cardiovascular Health ◽  
Critical Role ◽  
Potential Effect ◽  
Lipid Mediators ◽  
Physiological Effects ◽  
Therapeutic Approaches ◽  
The Impact ◽  
Long Chain

Cardiovascular disease remains a leading cause of mortality worldwide. Unresolved inflammation plays a critical role in cardiovascular diseases development. Specialized Pro-Resolving Mediators (SPMs), derived from long chain polyunsaturated fatty acids (LCPUFAs), enhances the host defense, by resolving the inflammation and tissue repair. In addition, SPMs also have anti-inflammatory properties. These physiological effects depend on the availability of LCPUFAs precursors and cellular metabolic balance. Most of the studies have focused on the impact of SPMs in adult cardiovascular health and diseases. In this review, we discuss LCPUFAs metabolism, SPMs, and their potential effect on cardiovascular health and diseases primarily focusing in neonates. A better understanding of the role of these SPMs in cardiovascular health and diseases in neonates could lead to the development of novel therapeutic approaches in cardiovascular dysfunction.

scholarly journals Acute small intestinal inflammation results in persistent lymphatic alterations

2018 ◽  
Vol 314 (3) ◽  
pp. G408-G417 ◽  
Author(s):  
Sonia Rehal ◽  
Matthew Stephens ◽  
Simon Roizes ◽  
Shan Liao ◽  
Pierre-Yves von der Weid
Keyword(s):  
Dendritic Cell ◽  
Lymphatic System ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Lymphatic Vessels ◽  
Lymphoid Tissues ◽  
Functional Changes ◽  
Increased Risk ◽  
Small Intestinal ◽  
Acute Ileitis

Inflammatory bowel disease (IBD) has a complex pathophysiology with limited treatments. Structural and functional changes in the intestinal lymphatic system have been associated with the disease, with increased risk of IBD occurrence linked to a history of acute intestinal injury. To examine the potential role of the lymphatic system in inflammation recurrence, we evaluated morphological and functional changes in mouse mucosal and mesenteric lymphatic vessels, and within the mesenteric lymph nodes during acute ileitis caused by a 7-day treatment with dextran sodium sulfate (DSS). We monitored whether the changes persisted during a 14-day recovery period and determined their potential consequences on dendritic cell (DC) trafficking between the mucosa and lymphoid tissues. DSS administration was associated with marked lymphatic abnormalities and dysfunctions exemplified by lymphangiectasia and lymphangiogenesis in the ileal mucosa and mesentery, increased mesenteric lymphatic vessel leakage, and lymphadenopathy. Lymphangiogenesis and lymphadenopathy were still evident after recovery from intestinal inflammation and correlated with higher numbers of DCs in mucosal and lymphatic tissues. Specifically, a deficit in CD103+ DCs observed during acute DSS in the lamina propria was reversed and further enhanced during recovery. We concluded that an acute intestinal insult caused alterations of the mesenteric lymphatic system, including lymphangiogenesis, which persisted after resolution of inflammation. These morphological and functional changes could compromise DC function and movement, increasing susceptibility to further gastrointestinal disease. Elucidation of the changes in mesenteric and intestinal lymphatic function should offer key insights for new therapeutic strategies in gastrointestinal disorders such as IBD. NEW & NOTEWORTHY Lymphatic integrity plays a critical role in small intestinal homeostasis. Acute intestinal insult in a mouse model of acute ileitis causes morphological and functional changes in mesenteric and intestinal lymphatic vessels. While some of the changes significantly regressed during inflammation resolution, others persisted, including lymphangiogenesis and altered dendritic cell function and movement, potentially increasing susceptibility to the recurrence of gastrointestinal inflammation.

scholarly journals SARS-CoV-2 and Acute Cerebrovascular Events: An Overview

2021 ◽  
Vol 10 (15) ◽  
pp. 3349
Author(s):  
Mehdi Ghasemi ◽  
Raffaella Pizzolato Umeton ◽  
Kiandokht Keyhanian ◽  
Babak Mohit ◽  
Nasrin Rahimian ◽  
...  
Keyword(s):  
Functional Outcomes ◽  
Case Reports ◽  
Critical Role ◽  
Epidemiological Studies ◽  
Therapeutic Approaches ◽  
Angiotensin Converting Enzyme 2 ◽  
Cerebrovascular Complications ◽  
Current State ◽  
Cerebrovascular Events ◽  
Brain Homeostasis

Since the coronavirus disease 2019 (COVID-19) pandemic, due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, accumulating evidence indicates that SARS-CoV-2 infection may be associated with various neurological manifestations, including acute cerebrovascular events (i.e., stroke and cerebral venous thrombosis). These events can occur prior to, during and even after the onset of COVID-19’s general symptoms. Although the mechanisms underlying the cerebrovascular complications in patients with COVID-19 are yet to be fully elucidated, the hypercoagulability state, inflammation and altered angiotensin-converting enzyme 2 (ACE-2) signaling in association with SARS-CoV-2 may play key roles. ACE-2 plays a critical role in preserving heart and brain homeostasis. In this review, we discuss the current state of knowledge of the possible mechanisms underlying the acute cerebrovascular events in patients with COVID-19, and we review the current epidemiological studies and case reports of neurovascular complications in association with SARS-CoV-2, as well as the relevant therapeutic approaches that have been considered worldwide. As the number of published COVID-19 cases with cerebrovascular events is growing, prospective studies would help gather more valuable insights into the pathophysiology of cerebrovascular events, effective therapies, and the factors predicting poor functional outcomes related to such events in COVID-19 patients.

scholarly journals The association between rs16917496 T/C polymorphism of SET8 gene and cancer risk in Asian populations: a meta-analysis

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Hui-Xia Wei ◽  
Guo-Xiang Tian ◽  
Ju-Kun Song ◽  
Lian-Jie Yang ◽  
Yu-Pei Wang
Keyword(s):  
Cancer Risk ◽  
Statistical Power ◽  
Genetic Model ◽  
Meta Analysis ◽  
Critical Role ◽  
Epidemiological Studies ◽  
Asian Populations ◽  
Online Databases ◽  
Cancer Types ◽  
Diversity Control

Epidemiological studies have demonstrated close associations between SET8 rs16917496 T/C polymorphism and cancer risk, but the results of published studies were not consistent. We therefore performed this meta-analysis to explore the associations between rs16917496 T/C polymorphism and cancer risk. Five online databases were searched. Odds ratios (ORs) with a 95% confidence interval (CI) were calculated to assess the association between rs16917496 T/C polymorphism and cancer risk. In addition, heterogeneity, accumulative, sensitivity analysis, and publication bias were conducted to check the statistical power. Overall, 13 publications involving 5878 subjects were identified according to included criteria. No significant cancer risk was observed in genetic model of SET8 rs16917496 T/C polymorphism in Asian populations (C vs. T: OR = 1.04, 95%CI = 0.88–1.23, P = 0.63%; TC vs. TT: OR = 1.17, 95%CI = 0.96–1.24, P = 0.11%; CC vs. TT: OR = 0.90, 95%CI = 0.60–1.37, P = 0.63; TC+CC vs. TT: OR = 1.11, 95%CI = 0.90–1.38, P = 0.33; CC vs. TT+TC: OR = 0.92, 95%CI = 0.65–1.30, P = 0.63). Furthermore, similar associations were found in the subgroup analysis of race diversity, control design, genotyping methods, and different cancer types. In summary, our meta-analysis indicated that the SET8 rs16917496 T/C polymorphism may not play a critical role in cancer development in Asian populations.

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