ER Stress and Disease: Toward Prevention and Treatment

Kaneko, Masayuki; Imaizumi, Kazunori; Saito, Atsushi; Kanemoto, Soshi; Asada, Rie; Matsuhisa, Koji; Ohtake, Yosuke

doi:10.1248/bpb.b17-00342

Cited by 89 publications

(51 citation statements)

References 49 publications

(54 reference statements)

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“…34 Therefore, alteration of the pro-apoptotic ER stress may be a potential strategy for the treatment of myocardial injury. ER stress is an important mechanism in the pathogenesis of cardiovascular diseases such as hypertensive, myocardial hypertrophy, atherosclerosis, myocardial ischaemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fan

Yao

et al. 2019

J Cellular Molecular Medi

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Fuziline, an aminoalcohol-diterpenoid alkaloid derived from Aconiti lateralis radix preparata, has been reported to have a cardioprotective activity in vitro. However, the potential mechanism of fuziline on myocardial protection remains unknown. In this study, we aimed to explore the efficacy and mechanism of fuziline on isoproterenol (ISO)-induced myocardial injury in vitro and in vivo. As a result, fuziline effectively increased cell viability and alleviated ISO-induced apoptosis. Meanwhile, fuziline significantly decreased the production of ROS, maintained mitochondrial membrane potential (MMP) and blocked the release of cytochrome C, suggesting that fuziline could play the cardioprotective role through restoring the mitochondrial function.Fuziline also could suppress ISO-induced endoplasmic reticulum (ER) stress via the PERK/eIF2α/ATF4/Chop pathway. In addition, using ROS scavenger NAC could decrease ISO-induced apoptosis and block ISO-induced ER stress, while PERK inhibitor GSK2606414 did not reduce the production of ROS, indicating that excess production of ROS induced by ISO triggered ER stress. And fuziline protected against ISO-induced myocardial injury by inhibiting ROS-triggered ER stress. Furthermore, fuziline effectively improved cardiac function on ISO-induced myocardial injury in rats. Western blot analysis also showed that fuziline reduced ER stress-induced apoptosis in vivo. Above these results demonstrated that fuziline could reduce ISO-induced myocardial injury in vitro and in vivo by inhibiting ROS-triggered ER stress via the PERK/eIF2α/ATF4/Chop pathway. K E Y W O R D Sapoptosis, ER stress, fuziline, isoproterenol, ROS | 1333 FAN et Al.

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Section: Discussionmentioning

confidence: 99%

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fan

Yao

et al. 2019

J Cellular Molecular Medi

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“…ER stress is associated with the accumulation of unfolded or misfolded proteins and is involved in various neurological disorders, such as cerebral ischemia, AD, and prion diseases [74].…”

Section: Endoplasmic Reticulum (Er) Stress Pathwaymentioning

confidence: 99%

Carnosine as a Possible Drug for Zinc-Induced Neurotoxicity and Vascular Dementia

Kawahara

Sadakane

Mizuno

et al. 2020

IJMS

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Increasing evidence suggests that the metal homeostasis is involved in the pathogenesis of various neurodegenerative diseases including senile type of dementia such as Alzheimer’s disease, dementia with Lewy bodies, and vascular dementia. In particular, synaptic Zn2+ is known to play critical roles in the pathogenesis of vascular dementia. In this article, we review the molecular pathways of Zn2+-induced neurotoxicity based on our and numerous other findings, and demonstrated the implications of the energy production pathway, the disruption of calcium homeostasis, the production of reactive oxygen species (ROS), the endoplasmic reticulum (ER)-stress pathway, and the stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) pathway. Furthermore, we have searched for substances that protect neurons from Zn2+-induced neurotoxicity among various agricultural products and determined carnosine (β-alanyl histidine) as a possible therapeutic agent for vascular dementia.

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“…Such misfolded proteins are frequently not processed and transported correctly, but are detected by the intracellular quality-control systems. This leads to retention of the protein in the endoplasmic reticulum and initiation of the "endoplasmicreticulum-associated protein degradation" (ERAD) pathway, which subjects them to proteasomemediated degradation [116,117].…”

Section: Small Molecules: Pharmacological Chaperones and Read-throughmentioning

confidence: 99%

Succinic Semialdehyde Dehydrogenase Deficiency: An Update

Didiášová¹,

Banning²,

Brennenstuhl³

et al. 2020

Preprint

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Succinic semialdehyde dehydrogenase deficiency (SSADH-D) is a genetic disorder that results from the aberrant metabolism of the neurotransmitter γ-amino butyric acid (GABA). The disease is caused by the impaired activity of the mitochondrial enzyme succinic semialdehyde dehydrogenase. SSADH-D manifests as varying degree of mental retardation, autism, ataxia and epileptic seizures, but the clinical picture is highly heterogeneous. So far, there is no approved therapy for this disease. In this review, we briefly summarize the molecular genetics of SSADH-D, the past and ongoing clinical trials and the emerging features of the molecular pathogenesis, including redox imbalance and mitochondrial dysfunction. The main aim of this review is to discuss the potential use of further therapy approaches that have so far not been tested in SSADH-D, such as pharmacological chaperones, read-through drugs and gene therapy. Special attention will also be paid to elucidating the role of patient advocacy organizations in facilitating research and in the communication between the researchers and the patients.

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ER Stress and Disease: Toward Prevention and Treatment

Cited by 89 publications

References 49 publications

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Fuziline alleviates isoproterenol‐induced myocardial injury by inhibiting ROS‐triggered endoplasmic reticulum stress via PERK/eIF2α/ATF4/Chop pathway

Carnosine as a Possible Drug for Zinc-Induced Neurotoxicity and Vascular Dementia

Succinic Semialdehyde Dehydrogenase Deficiency: An Update

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