Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Duan, Hongbo; Li, Yongqiang; Yan, Li; Huang, Yang; Wu, Jintao; Peng, Qian; Li, Bing; Wang, Shanling

doi:10.1016/j.yexcr.2015.05.003

Cited by 17 publications

(18 citation statements)

References 45 publications

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“…Atg5 haplodeficiency markedly decreases cytosolic autophagic vacuole formation induced by Ang II, increases nuclear factor-κB (NF-κB) activity and mitochondrial ROS production in macrophages, which contribute to subsequent cardiac inflammation and cardiac injury . These findings indicated that Ang II elevated ROS production and oxidative stress and induced autophagy, concomitant with cardiac injury, which also suggested that upregulation of autophagy may be a method of cardiac protection , Duan et al 2015.…”

Section: Autophagy-related Proteinmentioning

confidence: 79%

“…Regulator of calcineurin 1-1L (Rcan1-1L) promoted cell viability and mitochondrial autophagy in Ang II-treated human adult cardiac myocytes, with elevated ATG5 and LC3 expression and downregulation of phosphorylated p70S6K (Duan et al 2015). Additionally, Rcan1-1L significantly inhibited calcineurin/nuclear factor of activated T cells (NFAT) signaling, which may protect human cardiomyocytes from Ang II-activated oxidative stress through the induction of mitochondrial autophagy and may be a method of cardiac protection (Duan et al 2015).…”

Section: Regulation Of Various Key Moleculesmentioning

confidence: 99%

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The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

Zhou

Han

2016

Journal of Molecular Endocrinology

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Pathological cardiac hypertrophy is associated with nearly all forms of heart failure. It develops in response to disorders such as coronary artery disease, hypertension and myocardial infarction. Angiotensin II (Ang II) has direct effects on the myocardium and promotes hypertension. Chronic elevation of Ang II can lead to pathological cardiac hypertrophy and cardiac failure. Autophagy is an important process in the pathogenesis of cardiovascular diseases. Under physiological conditions, autophagy is an essential homeostatic mechanism to maintain the global cardiac structure function by ridding damaged cells or unwanted macromolecules and organelles. Dysregulation of autophagy may play an important role in Ang II-induced cardiac hypertrophy although conflicting reports on the effects of Ang II on autophagy and cardiac hypertrophy exist. Some studies showed that autophagy activation attenuated Ang II-induced cardiac dysfunction. Others suggested that inhibition of the Ang II induced autophagy should be protective. The discrepancies may be due to different model systems and different signaling pathway involved. Ang II-induced cardiac hypertrophy may be alleviated through regulation of autophagy. This review focuses on Ang II to highlight the molecular targets and pathways identified in the prevention and treatment of Ang II-induced pathological cardiac hypertrophy by regulating autophagy.

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Section: Autophagy-related Proteinmentioning

confidence: 79%

Section: Regulation Of Various Key Moleculesmentioning

confidence: 99%

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

Zhou

Han

2016

Journal of Molecular Endocrinology

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“…It has been reported that the activation of mTOR is required in immune cells [ 30 ] during proliferation. Furthermore, endotoxin-induced autophagy is a survival mechanism that drives proliferation of hepatocytes [ 31 ] and in cardiac tissues [ 32 ]. The central components of the cell survival pathway, including AKT and mTOR, sense cellular metabolic alterations and trigger cell survival [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

DNA polymerase gamma (Polγ) deficiency triggers a selective mTORC2 prosurvival autophagy response via mitochondria-mediated ROS signaling

et al. 2018

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Autophagy is a highly regulated evolutionarily conserved metabolic process induced by stress and energy deprivation. Here, we show that DNA polymerase gamma (Polγ) deficiency activates a selective prosurvival autophagic response via mitochondria-mediated reactive oxygen species (ROS) signaling and the mammalian target of rapamycin complex 2 (mTORC2) activities. In keratinocytes, Polγ deficiency causes metabolic adaptation that triggers cytosolic sensing of energy demand for survival. Knockdown of Polγ causes mitochondrial stress, decreases mitochondrial energy production, increases glycolysis, increases the expression of autophagy-associated genes, and enhances AKT phosphorylation and cell proliferation. Deficiency of Polγ preferentially activates mTORC2 formation to increase autophagy and cell proliferation, and knocking down Rictor abrogates these responses. Overexpression of Rictor, but not Raptor, reactivates autophagy in Polγ-deficient cells. Importantly, inhibition of ROS by a mitochondria-selective ROS scavenger abolishes autophagy and cell proliferation. These results identify Rictor as a critical link between mitochondrial stress, ROS, and autophagy. They represent a major shift in our understanding of the prosurvival role of the mTOR complexes and highlight mitochondria-mediated ROS as a prosurvival autophagy regulator during cancer development.

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“…The overexpression of the brain-specific RCAN1.1S isoform in mice promotes early age dependent memory and synaptic plasticity deficits, tau pathology, and dysregulation of dynamin-related protein 1 ( DRP1 ) activity associated with altered mitochondrial dynamics and oxidative stress (Wong et al 2015 ). Duan et al found that RCAN1 induces mitochondrial autophagy and improves cell survival in cardiomyocytes (Duan et al 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction in down syndrome: molecular mechanisms and therapeutic targets

Izzo

Mollo

Nitti

et al. 2018

Mol Med

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Trisomy of chromosome 21 (TS21) is the most common autosomal aneuploidy compatible with postnatal survival with a prevalence of 1 in 700 newborns. Its phenotype is highly complex with constant features, such as mental retardation, dysmorphic traits and hypotonia, and variable features including heart defects, susceptibility to Alzheimer’s disease (AD), type 2 diabetes, obesity and immune disorders. Overexpression of genes on chromosome-21 (Hsa21) is responsible for the pathogenesis of Down syndrome (DS) phenotypic features either in a direct or in an indirect manner since many Hsa21 genes can affect the expression of other genes mapping to different chromosomes. Many of these genes are involved in mitochondrial function and energy conversion, and play a central role in the mitochondrial dysfunction and chronic oxidative stress, consistently observed in DS subjects.Recent studies highlight the deep interconnections between mitochondrial dysfunction and DS phenotype. In this short review we first provide a basic overview of mitochondrial phenotype in DS cells and tissues. We then discuss how specific Hsa21 genes may be involved in determining the disruption of mitochondrial DS phenotype and biogenesis. Finally we briefly focus on drugs that affect mitochondrial function and mitochondrial network suggesting possible therapeutic approaches to improve and/or prevent some aspects of the DS phenotype.

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Rcan1-1L overexpression induces mitochondrial autophagy and improves cell survival in angiotensin II-exposed cardiomyocytes

Cited by 17 publications

References 45 publications

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

The role of autophagy in angiotensin II-induced pathological cardiac hypertrophy

DNA polymerase gamma (Polγ) deficiency triggers a selective mTORC2 prosurvival autophagy response via mitochondria-mediated ROS signaling

Mitochondrial dysfunction in down syndrome: molecular mechanisms and therapeutic targets

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