SOD1G93A Induces a Unique PSAP-Dependent Mitochondrial Apoptosis Pathway via Bax–Bak Interaction

Niu, Han; Chen, Xin; Fu, Xueqi; Zhang, Jingtian; Li, Guodong; Wang, Yuxiang; Song, Jiayue; Ma, Xiu-Wen; Hu, Chen; Xu, Xuemin; Zhang, Fuqiang; Zeng, Linlin

doi:10.32604/biocell.2021.015297

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…Mitochondria are responsible for the production of the majority of ROS as a by-product of cellular respiration, and homeostatic dysfunction [ 48 ]. The build-up of ROS results in the progression of neurodegeneration and has been closely linked to PD and AD and is also believed to play a key role in the pathogenesis of ALS [ 49 , 50 ]. In SOD1 -linked ALS, mitochondrial oxidative stress is caused by the production of mutant SOD1 [ 51 ].…”

Section: Molecular Mechanismsmentioning

confidence: 99%

Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?

Roberts

Theunissen

Mastaglia

et al. 2022

IJMS

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Amyotrophic lateral sclerosis (ALS) is the most common adult-onset motor neuron disease classified as both a neurodegenerative and neuromuscular disorder. With a complex aetiology and no current cure for ALS, broadening the understanding of disease pathology and therapeutic avenues is required to progress with patient care. Alpha-synuclein (αSyn) is a hallmark for disease in neurodegenerative disorders, such as Parkinson’s disease, Lewy body dementia, and multiple system atrophy. A growing body of evidence now suggests that αSyn may also play a pathological role in ALS, with αSyn-positive Lewy bodies co-aggregating alongside known ALS pathogenic proteins, such as SOD1 and TDP-43. This review endeavours to capture the scope of literature regarding the aetiology and development of ALS and its commonalities with “synucleinopathy disorders”. We will discuss the involvement of αSyn in ALS and motor neuron disease pathology, and the current theories and strategies for therapeutics in ALS treatment, as well as those targeting αSyn for synucleinopathies, with a core focus on small molecule RNA technologies.

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Section: Molecular Mechanismsmentioning

confidence: 99%

Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?

Roberts

Theunissen

Mastaglia

et al. 2022

IJMS

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show abstract

“…Western blotting showed that P-ATM, JNK, Bax, and STAT-3 were involved. The expression of P-ATM, JNK, and Bax was up-regulated, which suggested that they promote apoptosis through ROS generation downstream (Niu et al, 2021;Dandoti, 2021). The expression of STAT-3 was decreased, indicating the inhibition of its cell growth and survival promotion function.…”

Section: Discussionmentioning

confidence: 97%

Quercetin induced HepG2 cells apoptosis through ATM/JNK/STAT3 signaling pathways

LIU¹,

CHEN²,

Su³

et al. 2023

Biocell

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Liver cancer is the seventh most common malignant tumor in the world and is the second highest cause of death due to cancer. Quercetin, a flavonoid with low toxicity, widely exists in various fruits and vegetables. It has the potential to be a therapeutic agent against various cancers. This study aimed to demonstrate the anti-tumor effect of quercetin on HepG2 cells. Quercetin suppressed the HepG2 cell proliferation in a dose-dependent manner in cell viability assay. Induction of cell apoptosis was confirmed by apoptotic cells population (sub-G1 peak) detected by flow cytometer. A decrease in mitochondrial membrane potential and caspase-3 activation were also demonstrated in this study. Furthermore, quercetin induced HepG2 cell apoptosis through ROS-mediated phosphorylated ataxia-telangiectasia mutated, c-Jun Nterminal kinases, signal transducer, and activator of transcription 3 (STAT-3), and Bax signaling pathways. These resultssuggest that quercetin has the potential to become an effective drug against the tumor.

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BI1 Activates Autophagy and Mediates TDP43 to Regulate ALS Pathogenesis

Wang,

Yin

et al. 2024

Mol Neurobiol

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SOD1G93A Induces a Unique PSAP-Dependent Mitochondrial Apoptosis Pathway via Bax–Bak Interaction

Cited by 3 publications

References 25 publications

Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?

Synucleinopathy in Amyotrophic Lateral Sclerosis: A Potential Avenue for Antisense Therapeutics?

Quercetin induced HepG2 cells apoptosis through ATM/JNK/STAT3 signaling pathways

BI1 Activates Autophagy and Mediates TDP43 to Regulate ALS Pathogenesis

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