Endothelial Dysfunction and Venous Thrombosis

Poredoš, Pavel; Ježovnik, Mateja K

doi:10.1177/0003319717732238

Cited by 75 publications

(72 citation statements)

References 45 publications

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“… 31 Endothelial dysfunction induced by overexpressed proinflammatory cytokines, such as IL-1β and IL-6, partially attributes to the development of PAH. 32 , 33 Smooth muscle cells (SMCs) are responsible for regulating blood pressure and blood flow in healthy arteries, whereas inflammatory cytokine IL-1β modulates SMC phenotypes to an inflammatory state by inhibiting SMC differentiation marker genes and promoting proinflammatory factors. 34 Thus, in the present study, miR-340-5p suppressed PASMC proliferation and migration by downregulating IL-6 and IL-1β, thereby inhibiting thrombosis and PAH in the rat model.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Ou¹,

Zhang²,

Chen³

et al. 2020

Molecular Therapy - Nucleic Acids

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Pulmonary arterial hypertension (PAH) is a fatal cardiovascular disease that could eventually result in right ventricular failure. Recently, the roles of microRNAs (miRNAs) in PAH have been highlighted. The present study aims to investigate the effects of miRNA (miR)-340-5p on PAH induced by acute pulmonary embolism (APE) and the underlying mechanisms. miR-340-5p was lowly expressed, whereas interleukin 1β (IL-1β) and IL-6 were highly expressed in plasma of APE-PAH patients as compared to normal human plasma. Subsequently, IL-1β and IL-6 were confirmed to be two target genes of miR-340-5p using a dual-luciferase reporter gene assay. By conducting overexpression and rescue experiments, overexpression of miR-340-5p was evidenced to inhibit proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) and inflammation via reducing IL-1β and IL-6 levels. Meanwhile, miR-340-5p led to the blocked nuclear factor κB (NF-κB) pathway with reduced NF-κB p65, matrix metalloproteinase 2 (MMP2), and MMP9 expression in PASMCs. Finally, the ameliorative effect of miR-340-5p on pathological lesions was further verified in rat models of APE-PAH. Altogether, overexpressed miR-340-5p inhibited the inflammatory response, proliferation, and migration of PASMCs by downregulating IL-1β and IL-6, thereby suppressing the progression of APE-PAH. miR-340-5p therefore holds promise as an anti-inflammatory therapeutic target.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Ou¹,

Zhang²,

Chen³

et al. 2020

Molecular Therapy - Nucleic Acids

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show abstract

“…Endothelial dysfunction, which is described in seriously ill patients, promotes the release of pro‐thrombotic factors, including von Willebrand factor and P‐selectin and could predispose to thrombosis and thromboembolism in this clinical setting 79 . Additionally, systemic inflammation may occur particularly in predisposed patients leading to a progressive “thromboinflammatory” syndrome with consequent disseminated microvasculature involvement, multiorgan failure, or death 80 .…”

Section: Resultsmentioning

confidence: 99%

Worse progression of COVID‐19 in men: Is testosterone a key factor?

et al. 2020

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Background The novel severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) disease 2019 (COVID‐19) seems to have a worse clinical course among infected men compared with women, thus highlighting concerns about gender predisposition to serious prognosis. Therefore, androgens, particularly testosterone (T), could be suspected as playing a critical role in driving this excess of risk. However, gonadal function in critically ill men is actually unknown, mainly because serum T concentration is not routinely measured in clinical practice, even more in this clinical context. Objective To overview on possible mechanisms by which serum T levels could affect the progression of COVID‐19 in men. Methods Authors searched PubMed/MEDLINE, Web of Science, EMBASE, Cochrane Library, Google, and institutional websites for medical subject headings terms and free text words referred to “SARS‐CoV‐2,” “COVID‐19,” “testosterone,” “male hypogonadism,” “gender” “immune system,” “obesity,” “thrombosis” until May 19th 2020. Results T, co‐regulating the expression of angiotensin‐converting enzyme 2 and transmembrane protease serine 2 in host cells, may facilitate SARS‐CoV‐2 internalization. Instead, low serum T levels may predispose to endothelial dysfunction, thrombosis and defective immune response, leading to both impaired viral clearance and systemic inflammation. Obesity, one of the leading causes of severe prognosis in infected patients, is strictly associated with functional hypogonadism, and may consistently strengthen the aforementioned alterations, ultimately predisposing to serious respiratory and systemic consequences. Discussion and conclusion T in comparison to estrogen may predispose men to a widespread COVID‐19 infection. Low serum levels of T, which should be supposed to characterize the hormonal milieu in seriously ill individuals, may predispose men, especially elderly men, to poor prognosis or death. Further studies are needed to confirm these pathophysiological assumptions and to promptly identify adequate therapeutic strategies.

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“…BBB damage enables the translocation of cells including monocytes, erythrocytes, and other inflammatory cells into the extracellular space, thus triggering cascades of responses such as immunological or inflammatory reactions, cell injury, and fibrin or iron deposition. Researchers also suggest that prolonged elevated intracranial venous pressure can lead to hyalinosis and thickening of venous vessel wall, endothelial dysfunction, and arteriolar regulation impairment . Furthermore, in a previous study, it is interesting to notice that patients with extracranial venous drainage abnormalities displayed markedly decreased venous vasculature visibility on susceptibility‐weighted imaging (SWI) venography …”

Section: Proposed Pathophysiologymentioning

confidence: 99%

Understanding jugular venous outflow disturbance

Zhou

Ding

et al. 2018

CNS Neurosci Ther

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Extracranial venous abnormalities, especially jugular venous outflow disturbance, were originally viewed as nonpathological phenomena due to a lack of realization and exploration of their feature and clinical significance. The etiology and pathogenesis are still unclear, whereas a couple of causal factors have been conjectured. The clinical presentation of this condition is highly variable, ranging from insidious to symptomatic, such as headaches, dizziness, pulsatile tinnitus, visual impairment, sleep disturbance, and neck discomfort or pain. Standard diagnostic criteria are not available, and current diagnosis largely depends on a combinatory use of imaging modalities. Although few researches have been conducted to gain evidence-based therapeutic approach, several recent advances indicate that intravenous angioplasty in combination with stenting implantation may be a safe and efficient way to restore normal blood circulation, alleviate the discomfort symptoms, and enhance patients' quality of life. In addition, surgical removal of structures that constrain the internal jugular vein may serve as an alternative or adjunctive management when endovascular intervention is not feasible. Notably, discussion on every aspect of this newly recognized disease entity is in the infant stage and efforts with more rigorous designed, randomized controlled studies in attempt to identify the pathophysiology, diagnostic criteria, and effective approaches to its treatment will provide a profound insight into this issue.

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Endothelial Dysfunction and Venous Thrombosis

Cited by 75 publications

References 45 publications

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

RETRACTED: Overexpression of MicroRNA-340-5p Inhibits Pulmonary Arterial Hypertension Induced by APE by Downregulating IL-1β and IL-6

Worse progression of COVID‐19 in men: Is testosterone a key factor?

Understanding jugular venous outflow disturbance

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