Angiotensin Receptors and Autophagy

Steckelings, Ulrike Muscha; Unger, Thomas

doi:10.1161/hypertensionaha.109.131425

Cited by 5 publications

(5 citation statements)

References 8 publications

(13 reference statements)

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“…116 Regarding the renin-angiotensin-aldosterone system, autophagy is stimulated by angiotensin II via the type 1 receptor (AGTR1) but diminished via AGTR2 in neonatal rat cardiomyocytes overexpressing either AGTR1, AGTR2 or both receptors after adenoviral transduction. 117, 118 Cardiomyocytes derived from a genetic rat model of heart hypertrophy are more susceptible to AGTR1–induced autophagy, but also show a strong reduction of autophagy via AGTR2. 117 Therefore, besides their well-known favorable hemodynamic and neurohumoral effects in the treatment of heart failure (HF), AGTR1 antagonists may also downregulate excessive autophagic cell death and consequently preserve cardiomyocytes.…”

Section: Autophagy In the Genesis Of Cardiovascular Diseasesmentioning

confidence: 99%

Molecular Mechanisms of Autophagy in the Cardiovascular System

Gatica

Chiong

Lavandero

et al. 2015

Circulation Research

235

189

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Autophagy is a catabolic recycling pathway triggered by various intra- or extracellular stimuli that is conserved from yeast to mammals. During autophagy diverse cytosolic constituents are enveloped by double-membrane vesicles, autophagosomes, which later fuse with lysosomes or the vacuole in order to degrade their cargo. Dysregulation in autophagy is associated with a diverse range of pathologies including cardiovascular disease, the leading cause of death in the world. As such, there is great interest in identifying novel mechanisms that govern the cardiovascular response to disease-related stress. First described in failing hearts, autophagy within the cardiovascular system has been widely characterized in cardiomyocytes, cardiac fibroblasts, endothelial cells and vascular smooth muscle cells. In all cases, a window of optimal autophagic activity appears to be critical to the maintenance of cardiovascular homeostasis and function; excessive or insufficient levels of autophagic flux can each contribute to heart disease pathogenesis. Here we review the molecular mechanisms that govern autophagosome formation and analyze the link between autophagy and cardiovascular disease.

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Section: Autophagy In the Genesis Of Cardiovascular Diseasesmentioning

confidence: 99%

Molecular Mechanisms of Autophagy in the Cardiovascular System

Gatica

Chiong

Lavandero

et al. 2015

Circulation Research

235

189

View full text Add to dashboard Cite

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“…In contrast, several studies indicate a tissue-protective effect of the AT 2 receptor in cardiac disease because of its anti-fibrotic, anti-inflammatory, and anti-apoptotic features. Recently, it was shown that autophagy is promoted by angiotensin via the AT 1 receptor but is diminished via the AT 2 receptor in neonatal rat cardiomyocytes overexpressing either the AT 1 or the AT 2 or both receptors after adenoviral transfection [54,55]. Cardiomyocytes derived from a genetic model of disturbed heart growth in rats (hypertrophic heart rat) were more susceptible to AT 1 receptor-induced autophagy, but also showed a strong reduction of autophagic activity via the AT 2 receptor.…”

Section: Targeting Sirt1mentioning

confidence: 99%

Role of autophagy in heart failure associated with aging

2010

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Heart failure is a progressive disease, leading to reduced quality of life and premature death. Adverse ventricular remodeling involves changes in the balance between cardiomyocyte protein synthesis and degradation, forcing these myocytes in equilibrium between life and death. In this context, autophagy has been recognized to play a role in the pathophysiology of heart failure. At basal levels, autophagy performs housekeeping functions, maintaining cardiomyocyte function and ventricular mass. Autophagy also occurs in the failing human heart, and upregulation has been reported in animal models of pressure overload-induced heart failure. Although the factors that determine whether autophagy will be protective or detrimental are not well known, the level and duration of autophagy seem important. Autophagy may antagonize ventricular hypertrophy by increasing protein degradation, which decreases tissue mass. However, the rate of protective autophagy declines with age. The inability to remove damaged structures results in the progressive accumulation of 'garbage', including abnormal intracellular proteins aggregates and undigested materials such as lipofuscin. Eventually, the progress of these changes results in enhanced oxidative stress, decreased ATP production, collapse of the cellular catabolic machinery, and cell death. By contrast, in load-induced heart failure, the extent of autophagic flux can rise to maladaptive levels. Excessive autophagy induction leads to autophagic cell death and loss of cardiomyocytes and may contribute to the worsening of heart failure. Accordingly, the development of therapies that up-regulate the repair qualities of the autophagic process and down-regulate the cell death aspects would be of great value in the treatment of heart failure.

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“…The angiotensin receptor blockers (ARBs) and the angiotensin-converting enzyme (ACE) inhibitors are able to improve endothelial dysfunction and vascular inflammation in patients with hypertension and other cardiovascular diseases [ 167 ]. Furthermore, links between angiotensin signaling and autophagy exist in non-ECs [ 168 , 169 , 170 , 171 ]. Notably, the mechanisms of autophagy regulation by the angiotensin system imply mTOR, AMPK [ 172 ], and calpains [ 173 ].…”

Section: Current Diabetes Treatment May Prevent Endothelial Autophagy...mentioning

confidence: 99%

Endothelial Autophagy Dysregulation in Diabetes

Salemkour

Lenoir

2023

Cells

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Diabetes mellitus is a major public health issue that affected 537 million people worldwide in 2021, a number that is only expected to increase in the upcoming decade. Diabetes is a systemic metabolic disease with devastating macro- and microvascular complications. Endothelial dysfunction is a key determinant in the pathogenesis of diabetes. Dysfunctional endothelium leads to vasoconstriction by decreased nitric oxide bioavailability and increased expression of vasoconstrictor factors, vascular inflammation through the production of pro-inflammatory cytokines, a loss of microvascular density leading to low organ perfusion, procoagulopathy, and/or arterial stiffening. Autophagy, a lysosomal recycling process, appears to play an important role in endothelial cells, ensuring endothelial homeostasis and functions. Previous reports have provided evidence of autophagic flux impairment in patients with type I or type II diabetes. In this review, we report evidence of endothelial autophagy dysfunction during diabetes. We discuss the mechanisms driving endothelial autophagic flux impairment and summarize therapeutic strategies targeting autophagy in diabetes.

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Angiotensin Receptors and Autophagy

Cited by 5 publications

References 8 publications

Molecular Mechanisms of Autophagy in the Cardiovascular System

Molecular Mechanisms of Autophagy in the Cardiovascular System

Role of autophagy in heart failure associated with aging

Endothelial Autophagy Dysregulation in Diabetes

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