Placental Origins of Chronic Disease

Physiological Reviews, Journal Year: 2016, Volume and Issue: 96(4), P. 1509 - 1565

Published: Sept. 8, 2016

Epidemiological evidence links an individual's susceptibility to chronic disease in adult life events during their intrauterine phase of development. Biologically this should not be unexpected, for organ systems are at most plastic when progenitor cells proliferating and differentiating. Influences operating time can permanently affect structure functional capacity, the activity enzyme endocrine axes. It is now appreciated that such effects lay foundations a diverse array diseases become manifest many years later, often response secondary environmental stressors. Fetal development underpinned by placenta, forms interface between fetus its mother. All nutrients oxygen reaching must pass through organ. The placenta also has major functions, orchestrating maternal adaptations pregnancy mobilizing resources fetal use. In addition, it acts as selective barrier, creating protective milieu minimizing exposure hormones, glucocorticoids, xenobiotics, pathogens, parasites. shows remarkable capacity adapt adverse cues lessen impact on fetus. However, if placental function impaired, or exceeded, then may compromised. Here, we explore complex relationships phenotype developmental programming offspring. Ensuring optimal placentation offers new approach prevention disorders cardiovascular disease, diabetes, obesity, which epidemic proportions.

Language: Английский

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Emerging importance of satellite glia in nervous system function and dysfunction

Nature reviews. Neuroscience, Journal Year: 2020, Volume and Issue: 21(9), P. 485 - 498

Published: July 22, 2020

Satellite glial cells (SGCs) closely envelop cell bodies of neurons in sensory, sympathetic and parasympathetic ganglia. This unique organization is not found elsewhere the nervous system. SGCs sensory ganglia are activated by numerous types nerve injury inflammation. The activation includes upregulation fibrillary acidic protein, stronger gap junction-mediated SGC-SGC neuron-SGC coupling, increased sensitivity to ATP, downregulation Kir4.1 potassium channels cytokine synthesis release. There evidence that these changes contribute chronic pain augmenting neuronal activity consistent various rodent models likely also human pain. Therefore, understanding resulting abnormal interactions with could provide a mechanistic approach might be exploited therapeutically alleviation prevention We describe how altered four common pain: systemic inflammation (sickness behaviour), post-surgical pain, diabetic neuropathic post-herpetic

Language: Английский

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Clinical neurocardiology defining the value of neuroscience-based cardiovascular therapeutics

The Journal of Physiology, Journal Year: 2016, Volume and Issue: 594(14), P. 3911 - 3954

Published: April 27, 2016

The autonomic nervous system regulates all aspects of normal cardiac function, and is recognized to play a critical role in the pathophysiology many cardiovascular diseases. As such, value neuroscience-based therapeutics increasingly evident. This White Paper reviews current state understanding human neuroanatomy, neurophysiology, specific disease conditions, testing, risk stratification, neuromodulatory strategies mitigate progression

Language: Английский

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Autonomic Nervous System Dysfunction

Journal of the American College of Cardiology, Journal Year: 2019, Volume and Issue: 73(10), P. 1189 - 1206

Published: March 1, 2019

Language: Английский

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Heart–Brain Axis

Circulation Research, Journal Year: 2017, Volume and Issue: 120(3), P. 559 - 572

Published: Feb. 2, 2017

A complex interaction exists between the nervous and cardiovascular systems. large network of cortical subcortical brain regions control function via sympathetic parasympathetic outflow. dysfunction in one system may lead to changes other. The effects disease on have been widely studied; however, our understanding neurological disorders has only expanded past 2 decades. Various pathologies can a wide range alterations structure ranging from transient benign electrographic myocardial injury, cardiomyopathy, even cardiac death. In this article, we first review anatomy physiology central autonomic systems regard function. injury will be summarized, finally, commonly associated with manifestations.

Language: Английский

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Hypertension and cardiac arrhythmias: a consensus document from the European Heart Rhythm Association (EHRA) and ESC Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulación Cardíaca y Electrofisiología (SOLEACE)

EP Europace, Journal Year: 2017, Volume and Issue: 19(6), P. 891 - 911

Published: June 1, 2017

Hypertension is a common cardiovascular risk factor leading to heart failure (HF), coronary artery disease, stroke, peripheral disease and chronic renal insufficiency. Hypertensive can manifest as many cardiac arrhythmias, most commonly being atrial fibrillation (AF). Both supraventricular ventricular arrhythmias may occur in hypertensive patients, especially those with left hypertrophy (LVH) or HF. Also, some of the antihypertensive drugs used reduce blood pressure, such thiazide diuretics, result electrolyte abnormalities (e.g. hypokalaemia, hypomagnesemia), further contributing whereas effective control pressure prevent development AF. In recognizing this close relationship between hypertension European Heart Rhythm Association (EHRA) Society Cardiology (ESC) Council on convened Task Force, representation from (HRS), Asia-Pacific (APHRS), Sociedad Latinoamericana de Estimulación Cardíaca y Electrofisiología (SOLEACE), remit comprehensively review available evidence publish joint consensus document provide up-to-date recommendations for use clinical practice. The ultimate judgment regarding care particular patient must be made by healthcare provider light all circumstances presented that patient.

Language: Английский

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The autonomic nervous system and cardiac arrhythmias: current concepts and emerging therapies

Nature Reviews Cardiology, Journal Year: 2019, Volume and Issue: 16(12), P. 707 - 726

Published: June 13, 2019

Language: Английский

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NLRP3 Inflammasome Activation Through Heart-Brain Interaction Initiates Cardiac Inflammation and Hypertrophy During Pressure Overload

Circulation, Journal Year: 2022, Volume and Issue: 147(4), P. 338 - 355

Published: Nov. 28, 2022

Mechanical stress on the heart, such as high blood pressure, initiates inflammation and causes hypertrophic heart disease. However, regulatory mechanism of its role in stressed remain unclear. IL-1β (interleukin-1β) is a proinflammatory cytokine that cardiac hypertrophy failure. Here, we show neural signals activate NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3) inflammasome for production to induce adaptive heart.C57BL/6 mice, knockout mouse strains P2RX7 (P2X purinoceptor 7), adrenergic neuron-specific mice SLC17A9, secretory vesicle protein responsible storage release ATP, were used analysis. Pressure overload was induced by transverse aortic constriction. Various animal models used, including pharmacological treatment with apyrase, lipopolysaccharide, 2'(3')-O-(4-benzoylbenzoyl)-ATP, MCC950, anti-IL-1β antibodies, clonidine, pseudoephedrine, isoproterenol, bisoprolol, left stellate ganglionectomy, ablation afferent nerves capsaicin. Cardiac function morphology, gene expression, myocardial caspase-1 activity, extracellular ATP level assessed. In vitro experiments performed using primary cardiomyocytes fibroblasts from rat neonates human microvascular endothelial cell line. Cell surface area proliferation assessed.Genetic disruption resulted significant loss production, hypertrophy, contractile during pressure overload. A bone marrow transplantation experiment revealed an essential nonimmune cells phenotype. Pharmacological depletion or genetic P2X7 receptor suppressed activity overload, indicating important ATP/P2X7 axis hypertrophy. Extracellular changes NLRP3- IL-1β-dependent manner vitro. Manipulation sympathetic nervous system suggested efferent main source ATP. Depletion nerves, lipophilic β-blocker reduced level, inhibited activation, overload.Cardiac are regulated heart-brain interaction. Controlling might be hypertensive

Language: Английский

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Myocardial ischemia/reperfusion: Translational pathophysiology of ischemic heart disease

Med, Journal Year: 2024, Volume and Issue: 5(1), P. 10 - 31

Published: Jan. 1, 2024

Ischemic heart disease is the greatest health burden and most frequent cause of death worldwide. Myocardial ischemia/reperfusion pathophysiological substrate ischemic disease. Improvements in prevention treatment have reduced mortality developed countries over last decades, but further progress now stagnant, morbidity from developing are increasing. Significant problems remain to be resolved require a better understanding. The present review attempts briefly summarize state art myocardial research, with view on both its coronary vascular aspects, define cutting edges where mechanistic knowledge needed facilitate translation clinical practice.

Language: Английский

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Aging impairs the neurovascular interface in the heart

Science, Journal Year: 2023, Volume and Issue: 381(6660), P. 897 - 906

Published: Aug. 24, 2023

Aging is a major risk factor for impaired cardiovascular health. Because the aging myocardium characterized by microcirculatory dysfunction, and because nerves align with vessels, we assessed impact of on cardiac neurovascular interface. We report that reduces nerve density in ventricle dysregulates vascular-derived neuroregulatory genes. down-regulates microRNA 145 (miR-145) derepresses neurorepulsive semaphorin-3A. miR-145 deletion, which increased

Language: Английский

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