Pulmonary Effects of Chronic Elevation in Microvascular Pressure Differ Between Hypertension and Myocardial Infarct Induced Heart Failure

Dixon, Dani‐Louise; Griggs, Kim; Pasquale, Carmine G. De; Bersten, Andrew D.

doi:10.1016/j.hlc.2014.08.009

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…Hypertension may result in several complications, including myocardial infarction, coronary artery disease, and heart failure [30, 31]. In hypertension, the reduced elastin content and increased collagen deposition are the typical characteristics of vascular mechanical property changes [2].…”

Section: Discussionmentioning

confidence: 99%

MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

Chen

Zhengqing³

et al. 2021

J Vasc Res

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Hypertension is considered a risk factor for a series of systematic diseases. Known factors including genetic predisposition, age, and diet habits are strongly associated with the initiation of hypertension. The current study aimed to investigate the role of miR-22-3p in hypertension. In this study, we discovered that the miR-22-3p level was significantly decreased in the thoracic aortic vascular tissues and aortic smooth muscle cells (ASMCs) of spontaneously hypertensive rats. Functionally, the overexpression of miR-22-3p facilitated the switch of ASMCs from the synthetic to contractile phenotype. To investigate the underlying mechanism, we predicted 11 potential target mRNAs for miR-22-3p. After screening, chromodomain helicase DNA-binding 9 (CHD9) was validated to bind with miR-22-3p. Rescue assays showed that the co-overexpression of miR-22-3p and CHD9 reversed the inhibitory effect of miR-22-3p mimics on cell proliferation, migration, and oxidative stress in ASMCs. Finally, miR-22-3p suppressed vascular remodeling and oxidative stress in vivo. Overall, miR-22-3p regulated ASMC phenotype switch by targeting CHD9. This new discovery provides a potential insight into hypertension treatment.

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Section: Discussionmentioning

confidence: 99%

MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

Chen

Zhengqing³

et al. 2021

J Vasc Res

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“…West and colleagues (6–9) have described the phenomenon of “stress failure” of pulmonary capillaries to explain severe endothelial capillary breakdown in response to high pulmonary vascular pressures that can lead to high-altitude pulmonary-, neurogenic-, and left heart failure-associated pulmonary edema (10–13). It is known that disruption of the thin capillary–alveolar barrier (<1 µm) comprising alveolar epithelial cell and endothelial cell (EC) monolayers can be induced by high lung capillary pressures (14, 15); however, it is not known whether endothelial barrier breakdown induced by the pressure rise is the result of activation of intrinsic endothelial signaling pathways that cause disassembly of AJs or release of permeability-increasing mediators.…”

mentioning

confidence: 99%

Endothelial cell Piezo1 mediates pressure-induced lung vascular hyperpermeability via disruption of adherens junctions

Friedrich

Hong

Xiong

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

179

144

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Increased pulmonary microvessel pressure experienced in left heart failure, head trauma, or high altitude can lead to endothelial barrier disruption referred to as capillary “stress failure” that causes leakage of protein-rich plasma and pulmonary edema. However, little is known about vascular endothelial sensing and transduction of mechanical stimuli inducing endothelial barrier disruption. Piezo1, a mechanosensing ion channel expressed in endothelial cells (ECs), is activated by elevated pressure and other mechanical stimuli. Here, we demonstrate the involvement of Piezo1 in sensing increased lung microvessel pressure and mediating endothelial barrier disruption. Studies were made in mice in which Piezo1 was deleted conditionally in ECs (Piezo1iΔEC), and lung microvessel pressure was increased either by raising left atrial pressure or by aortic constriction. We observed that lung endothelial barrier leakiness and edema induced by raising pulmonary microvessel pressure were abrogated inPiezo1iΔECmice. Piezo1 signaled lung vascular hyperpermeability by promoting the internalization and degradation of the endothelial adherens junction (AJ) protein VE-cadherin. Breakdown of AJs was the result of activation of the calcium-dependent protease calpain and degradation of the AJ proteins VE-cadherin, β-catenin, and p120-catenin. Deletion of Piezo1 in ECs or inhibition of calpain similarly prevented reduction in the AJ proteins. Thus, Piezo1 activation in ECs induced by elevated lung microvessel pressure mediates capillary stress failure and edema formation secondary to calpain-induced disruption of VE-cadherin adhesion. Inhibiting Piezo1 signaling may be a useful strategy to limit lung capillary stress failure injury in response to elevated vascular pressures.

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“…Повышение давления в системе легочной артерии встречается при многих заболеваниях внутренних ор-ганов и является закономерным этапом прогрессиро-вания ХСН [8]. Распространенность ЛГ у больных с си-столической ХСН может достигать 60% [9].…”

Section: Discussionunclassified

Lung Function Parameters in Patients with Dilated Cardiomyopathy Complicated by Pulmonary Hypertension

Абдуллаев

Ahmatov

Марданов

et al. 2016

Racionalʹnaâ farmakoterapiâ v kardiologii

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1 Республиканский специализированный центр кардиологии Узбекистан, 100052, Ташкент, ул. Осиё, 4 2 Государственный научно-исследовательский центр профилактической медицины Россия, 101990, Москва, Петроверигский пер., 10, стр.3Цель. Изучить особенности клинико-морфофункциональных показателей и характеристики функции внешнего дыхания у больных дилата-ционной кардиомиопатией (ДКМП) с легочной гипертензией (ЛГ) и без нее. Материал и методы. Обследован 91 больной c идиопатической ДКМП (34 женщины и 57 мужчин; средний возраст 46,4±13,7 лет). 25 (27,4%) больных имели правожелудочковую ДКМП (ПЖ ДКМП). Всем пациентам проводили тест 6-минутной ходьбы (ТШХ), стандартную ЭКГ в 12 отведениях, оценку клинического состояния (по шкале оценки клинического состояния; ШОКС), трансторакальную эхокардиогра-фию, спирографию. Пациенты с ЛГ (n=48) составили I группу. Вторую группу составили больные без ЛГ (n=43). Количество пациентов с ПЖ ДКМП в каждой группе составило 11 (23%) и 14 (32,5%), соответственно. Результаты. Систолическое давление в легочной артерии (СДЛА) у больных I группы составило 48,1±10,7 мм рт. ст. (у 71% -1 степень ЛГ, 29% -2 степень). Также у больных I группы выявлено значимое снижение практически всех скоростных показателей функции внешнего ды-хания. Выявлена обратная зависимости между СДЛА и индексом Тиффно (р=0,03) у больных I группы, и положительная корреляция меж-ду форсированной жизненной емкостью легких (53,17±9,21%) и длиной пройденной дистанции в ТШХ (206,7±80,3 м; p=0,017). Заключение. Синдром ЛГ довольно часто отягощает течение ДКМП. В качестве показателей нарушений функции внешнего дыхания у боль-ных ДКМП выступают объем форсированного выдоха за первую секунду, индекс Тиффно, а также некоторые скоростные показатели.Ключевые слова: дилатационная кардиомиопатия, правый желудочек, легочная гипертензия, функция внешнего дыхания. Aim. To study clinical and morphofunctional indicators of respiratory function in patients with dilated cardiomyopathy (DCM) with and without pulmonary hypertension (PH). Material and methods. 91 patients with idiopathic DCM (34 women and 57 men; mean age of 46.4±13.7 years) were included into the study. 25 (27.4%) patients had right ventricular DCM (RV DCM). 6-minute walking test (6MWT), the standard 12-lead ECG, spirography, echocardiography were performed in all patients. PH occurred in 48 of DCM patients (Group I) and 43 DCM patients had no PH (Group II). A number of patients with RV DCM in Groups I and II was 11 (23%) and 14 (32.5%), respectively. Results. Pulmonary artery systolic pressure (PASP) in group I was 48.1±10.7 mmHg (in 71% of the patients -degree 1 of PH, and in 29% -degree 2). A significant decrease in the majority of speed indicators of respiratory functions was found in Group I. The inverse relationship between PASP and Tiffno index (p=0.03) and a positive correlation between forced vital capacity (53.17±9.21%) and 6MWT distance (206.7±80.3 m; p=0.017) were found in patients of Group I. Conclusion. PH syndrome often aggravates the DCM course. Forced expiratory volu...

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Pulmonary Effects of Chronic Elevation in Microvascular Pressure Differ Between Hypertension and Myocardial Infarct Induced Heart Failure

Cited by 6 publications

References 34 publications

MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

Endothelial cell Piezo1 mediates pressure-induced lung vascular hyperpermeability via disruption of adherens junctions

Lung Function Parameters in Patients with Dilated Cardiomyopathy Complicated by Pulmonary Hypertension

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