The endoplasmic reticulum stress-autophagy pathway is involved in apelin-13-induced cardiomyocyte hypertrophy in vitro

Xie, Feng; Wu, Di; Huang, Shifang; Cao, Jun; Li, He-ning; He, Lu; Liu, Meiqing; Li, Lanfang; Chen, Linxi

doi:10.1038/aps.2017.97

Cited by 38 publications

(32 citation statements)

References 41 publications

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“…For example, a previous study demonstrates that apelin reduces oxidative stress and prevents pressure-overloadinduced left ventricular hypertrophy 44 . By contrast, there is increasing evidence proving that apelin-13 induces cardiac hypertrophy by increasing the production of ROS and the expression levels of NADPH oxidases in vivo and in vitro [45][46][47] . In addition, apelin/APJ in paraventricular nucleus is found to induce long-term high BP and renal sympathetic nerve activity via increasing oxidative stress 37,48 .…”

Section: Discussionmentioning

confidence: 97%

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ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway

Chen

Liu

et al. 2020

Cell Death Dis

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ELABELA (ELA), a 32-residue hormone peptide abundantly expressed in adult kidneys, has been identified as a novel endogenous ligand for APJ/Apelin receptor. The aim of this study was to investigate the role of ELA in deoxycorticosterone acetate (DOCA)/salt-induced hypertension and further explore the underlying mechanism. In DOCA/salt-treated rats, the mRNA level of ELA greatly decreased in the renal medulla. Next, overexpression of ELA in the kidney was found to attenuate DOCA/salt-induced hypertension and renal injury, including lower blood pressure, reversed glomerular morphological damage, decreased blood urea nitrogen (BUN), and blocked the accumulation of fibrotic markers. Mechanistically, ELA overexpression inhibited renal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and subsequent reactive oxygen species (ROS) production, thus resulted in the blockade of formation and activation of Nod-like receptor protein 3 (NLRP3) inflammasome. The inhibitory effects of ELA on Aldosterone-stimulated NADPH oxidase/ROS/NLRP3 inflammasome pathway were confirmed in the human renal tubular cells. Furthermore, our in vivo and in vitro results showed that the deficiency of the apelin receptor APJ did not influence the antihypertensive effect and blockage to NADPH oxidase/ROS/NLRP3 pathway of ELA. Moreover, in heterozygous ELA knockout mice (ELA+/−), the ELA deficiency remarkably accelerated the onset of DOCA/salt-induced hypertension. Our data demonstrate that ELA prevents DOCA/salt-induced hypertension by inhibiting NADPH oxidase/ROS/NLRP3 pathway in the kidney, which is APJ independent. Pharmacological targeting of ELA may serve as a novel therapeutic strategy for the treatment of hypertensive kidney disease.

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Section: Discussionmentioning

confidence: 97%

“…In addition, it is known that the regulatory effects of apelin on oxidative stress are conducted by binding to its receptor APJ in most experimental conditions 37,46,47 . As another endogenous ligand, it is still unclear whether ELA is dependent on APJ to suppress DOCA/salt-induced NADPH oxidase/ROS/NLRP3 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway

Chen

Liu

et al. 2020

Cell Death Dis

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“…The unfolded protein response is a prominent feature of ER stress (25). ER stress also contributes to apoptosis and hypertrophic growth of cardiomyocytes (26,27). Attenuation of ER stress prevents cardiomyocyte senescence and improves cardiomyocyte contractility cardiac function (28,29).…”

Section: Er Stressmentioning

confidence: 99%

Cardiomyocyte Senescence and Cellular Communications Within Myocardial Microenvironments

2020

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Cardiovascular diseases have become the leading cause of human death. Aging is an independent risk factor for cardiovascular diseases. Cardiac aging is associated with maladaptation of cellular metabolism, dysfunction (or senescence) of cardiomyocytes, a decrease in angiogenesis, and an increase in tissue scarring (fibrosis). These events eventually lead to cardiac remodeling and failure. Senescent cardiomyocytes show the hallmarks of DNA damage, endoplasmic reticulum stress, mitochondria dysfunction, contractile dysfunction, hypertrophic growth, and senescence-associated secreting phenotype (SASP). Metabolism within cardiomyocytes is essential not only to fuel the pump function of the heart but also to maintain the functional homeostasis and participate in the senescence of cardiomyocytes. The senescence of cardiomyocyte is also regulated by the non-myocytes (endothelial cells, fibroblasts, and immune cells) in the local microenvironment. On the other hand, the senescent cardiomyocytes alter their phenotypes and subsequently affect the non-myocytes in the local microenvironment and contribute to cardiac aging and pathological remodeling. In this review, we first summarized the hallmarks of the senescence of cardiomyocytes. Then, we discussed the metabolic switch within senescent cardiomyocytes and provided a discussion of the cellular communications between dysfunctional cardiomyocytes and non-myocytes in the local microenvironment. We also addressed the functions of metabolic regulators within non-myocytes in modulating myocardial microenvironment. Finally, we pointed out some interesting and important questions that are needed to be addressed by further studies.

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“…Apelin exerts this effect by activation of ERK and Akt pathways (Zeng et al, ). However, there are some reports showing that apelin‐13 increases the level of ROS in different cells (Li et al, ; Xie et al, ). Apelin also can improve the efficacy of cell therapy for peripheral artery disease (PAD).…”

Section: Apelin and Stem Cells: Effect On Stem Cell Propertiesmentioning

confidence: 99%

Apelin and stem cells: the role played in the cardiovascular system and energy metabolism

Esmaeili

Bandarian

Esmaeili

et al. 2019

Cell Biology International

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Apelin, a member of the adipokine family, is widely distributed in the body and exerts cytoprotective effects on many organs. Apelin isoforms are involved in different physiological processes, including regulation of the cardiovascular system, cardiac contractility, angiogenesis, and energy metabolism. Several investigations have been performed to study the effect of apelin on stem cell therapy. This review aims to summarize the literature representing the effects of apelin on stem cell properties. Furthermore, this review discusses the therapeutic potential of apelin-treated stem cells for cardiovascular diseases and demonstrates the effect of stem cells overexpressing apelin on energy metabolism. Stem cells with their unique characteristics play a crucial role in the maintenance of tissue integrity. These cells participate in tissue regeneration via multiple mechanisms. Although preclinical and clinical studies have demonstrated the therapeutic potential of stem cells in various diseases, their application in regenerative medicine has not been efficient. A number of strategies such as genetic modification or treatment of stem cells with different factors have been used to improve the efficacy of cell therapy and to increase their survival after transplantation. This article reviews the effect of apelin treatment on the efficacy of cell therapy.

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The endoplasmic reticulum stress-autophagy pathway is involved in apelin-13-induced cardiomyocyte hypertrophy in vitro

Cited by 38 publications

References 41 publications

ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway

ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway

Cardiomyocyte Senescence and Cellular Communications Within Myocardial Microenvironments

Apelin and stem cells: the role played in the cardiovascular system and energy metabolism

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