Novel insights into the role of urotensin II in cardiovascular disease

Pereira-Castro, João; Brás-Silva, Carmen; Fontes-Sousa, Ana Patrícia

doi:10.1016/j.drudis.2019.08.005

Cited by 20 publications

(20 citation statements)

References 123 publications

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“…6) UII is widely expressed in the cardiovascular system, with evidence for expression of a UII protein or gene in vascular smooth muscle cells, endothelial cells, endocardial endothelial cells, inflammatory cells, cardiomyocytes, and fibroblasts. [6][7][8][9][11][12][13][14][15] These findings provide strong evidence for transcriptional and translational regulation of the UII system locally within the cardiovascular system. In a physical state, low levels of UII could be detected in plasma, supporting the hypothesis that it acts as an autocrine and/or paracrine agent.…”

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confidence: 60%

“…[6][7][8] In the cardiovascular system, many reports indicated that UII might be implicated in cardiovascular regulation, with promising therapeutic applications based on UT receptor antagonism. 9) UII has strong effects on vascular activity and can induce contraction of rat thoracic aorta 6) and dilate human pulmonary artery, and reduce abdominal vascular resistance. 10) Moreover, UII administration to human subjects induced ST segment changes in the electrocardiogram observed in myocardial ischemia.…”

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confidence: 99%

“…In response to cardiovascular risk factors and pathological changes such as hypertension, obesity, diabetes, aging, atherosclerosis, cardiac hypertrophy, and heart failure, the expression of UII could be increased not only in the cardiovascular system but also in plasma, sug-gesting the pathophysiological roles of UII in cardiovascular diseases. [6][7][8][9][11][12][13][14][15][16][17][18] The expression of UII has been demonstrated to be increased in cardiac tissue from patients with congestive heart failure, which positively correlates with disease severity and inversely with cardiac function. 16) Recently, serum UII level has been reported to be markedly elevated in patients with hypertrophic cardiomyopathy and acute myocardial infarction, 17,18) suggesting that UII might be a novel biomarker parameter that has clinical use in patients with these diseases.…”

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confidence: 99%

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Urotensin II Induces Cardiac Fibrosis through the TGF-β/Smad Signaling Pathway during the Development of Cardiac Hypertrophy

Liang

Ding

et al. 2021

Int. Heart J.

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Myocardial fibrosis is an important pathological phenomenon of cardiac remodeling that is induced by hypertension, myocardial ischemia, valvular heart disease, hypertrophic cardiomyopathy, and other heart diseases and can progress to heart failure. Urotensin II (UII) is regarded as a cardiovascular autacoid/hormone that is not only the most potent vasoconstrictor in mammals but also involved in cardiac remodeling. However, the molecular mechanisms responsible for UII-induced cardiac fibrosis have not yet been fully elucidated. Therefore, we aimed to investigate the effect of UII on myocardial fibrosis in cardiac hypertrophy and the mechanism of UII-induced cardiac fibrosis. Cardiac tissue from mice subjected to Transverse aortic constriction (TAC) was collected. Cardiac hypertrophy, myocardial fibrosis, and the expression of UII protein were assessed using echocardiography and pathological and molecular biological analyses. The effect of UII on fibrosis was evaluated in UII-treated mice and isolated rat primary cardiac fibroblasts, and the results indicated that UII induced significant myocardial fibrosis and increases in the proliferation and fibrotic responses both in mice and cultured fibroblasts. Mechanistically, UII treatment induced activation of the TGF-β/Smad signaling pathway, which was suppressed by the UII receptor antagonist. In conclusion, UII plays critical roles in cardiac fibrosis by modulating the TGF-β/Smads signaling pathway, which may be a promising therapeutic target in hypertrophic cardiomyopathy and related problems, such as cardiac remodeling and heart failure.

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confidence: 60%

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confidence: 99%

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confidence: 99%

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Urotensin II Induces Cardiac Fibrosis through the TGF-β/Smad Signaling Pathway during the Development of Cardiac Hypertrophy

Liang

Ding

et al. 2021

Int. Heart J.

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“…Urotensin II (UII) is the most potent vasoactive substance [3] and its binding to the G protein-coupled receptor GPR14 (also named as UT) produces a variety of biological effects and is involved in multiple cardiovascular diseases, such as essential hypertension, coronary heart disease, congestive heart failure, diabetes mellitus and renal failure [3][4][5]. In addition, recent evidence suggested UII contributes to the development of atherosclerotic cardiovascular diseases [6][7][8][9]. For example, UII induces monocytes chemotaxis and contributes to the recruitment of monocyte expressing the UT receptor to the atherosclerotic lesions [10].…”

Section: Introductionmentioning

confidence: 99%

Dynamic Changes in Plasma Urotensin II and Its Correlation With Plaque Stability

Yin

Wang

et al. 2021

Journal of Cardiovascular Pharmacology

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Background: Urotensin II (UII) is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaque is undetermined. The purpose of this study was to observe the dynamic change of plasma UII and analyze its relationship with the stability of atherosclerotic plaques. Methods: The plasma UII concentration in patients with acute coronary syndrome (ACS) was detected. A vulnerable plaque model was established by local transfection of a recombinant P53 adenovirus into plaques of rabbits fed with a high-cholesterol diet and subjected to balloon injury, to evaluate the stability of the atherosclerotic plaques.Results: Our results showed that the level of plasma UII was increased in ACS patients compared with healthy subjects. However, it was signi cantly decreased in ST-segment elevation myocardial infarction patients (STEMI) and increased again in acute myocardial infarction (AMI) patients that were discharged after three months. UII dynamic change and its correlation with plaques stabilities were further veri ed in rabbit with atherosclerotic vulnerable plaque. The UII level in rabbits was signi cantly decreased after P53 gene transfection which can lead to of plaque instability. Conclusions:In conclusion, the level of plasma UII was signi cantly decreased in ACS with STEMI, which may serve as a reliable biological marker to re ect the progression and stability of atherosclerotic plaques.

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“…Urotensin-II is the most potent mammalian vasoconstrictor discovered till now, produced and synthesized within endothelial cells of many arteries and venous cell walls. UII has been engaged with diabetes disease and complications through its activity on the peripheral vascular bed [10]. UII is a pluripotent peptide that plays essential roles in the development of insulin-resistance.…”

Section: Introductionmentioning

confidence: 99%

Association of Serum Urotensin-II Levels with Insulin Resistance and Endothelin-I in Type-II Diabetes Mellitus Patients

Khidhir

Mahmud

Maulood

2021

eijs

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Urotensin-II (UII), a pluripotent vasoactive cyclic peptide, exhibits the progression of cardiovascular diseases and the glucose metabolic disorder of insulin resistance. Type 2 Diabetes Mellitus (T2DM) is entirely associated with insulin resistance. This study aimed to demonstrate the association of UII with insulin resistance in diabetic and non-diabetic subjects. A total of 73 male and female subjects aged 40-60 years were recruited in this case-control study. They included 35 non- diabetic subjects with a body mass index of (BMI) ≤ 25 and 38 patients with Diabetes Mellitus and BMI ≥ 25. UII levels were assessed beside other vasoactive and clinical parameters. The results revealed that patients with T2DM had elevated UII and Endothelin-I (ET-I) levels, along with positive correlations with the insulin-resistance marker of Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), blood pressure (BP), fasting blood glucose (FBG), hemoglobin A1c (HbA1C), and asymmetric dimethylarginine (ADMA). Results from stepwise multiple regressions indicated that UII correlated positively with the increases in the levels of serum cholesterol, ET-I, urea, ADMA, and FBG. This study concludes that the increase in UII level has a positive relation with insulin-resistance and the increase in ET-I level. However, UII could inhibit glucose-induced insulin secretion and, hence, can be utilized as a marker for T2DM and its complications through inflammatory microangiopathy.

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Novel insights into the role of urotensin II in cardiovascular disease

Cited by 20 publications

References 123 publications

Urotensin II Induces Cardiac Fibrosis through the TGF-β/Smad Signaling Pathway during the Development of Cardiac Hypertrophy

Urotensin II Induces Cardiac Fibrosis through the TGF-β/Smad Signaling Pathway during the Development of Cardiac Hypertrophy

Dynamic Changes in Plasma Urotensin II and Its Correlation With Plaque Stability

Association of Serum Urotensin-II Levels with Insulin Resistance and Endothelin-I in Type-II Diabetes Mellitus Patients

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