Mitochondrial Mechanisms of Apoptosis and Necroptosis in Liver Diseases

Chu, Qingfei; Gu, Xinyu; Zheng, Qiuxian; Wang, Jing; Zhu, Haihong

doi:10.1155/2021/8900122

Cited by 27 publications

(16 citation statements)

References 76 publications

(78 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Once mitochondrial membrane depolarization occurred and MMP collapsed, cytochrome c would be released from the intermembrane of the mitochondria into the cytoplasm [ 25 ]. KWM treatment induced translocation of cytochrome c , which was proved by examination of the cytochrome c protein level in the cytoplasm and the mitochondria, respectively.…”

Section: Resultsmentioning

confidence: 99%

A Mulberry Diels-Alder-Type Adduct, Kuwanon M, Triggers Apoptosis and Paraptosis of Lung Cancer Cells through Inducing Endoplasmic Reticulum Stress

Luan

Zheng

et al. 2023

IJMS

View full text Add to dashboard Cite

The mulberry tree (Morus alba) has been cultivated in China for thousands of years. Mulberry Diels-Alder-type adducts (MDAAs) are characteristic constituents of the genus Morus. The unique structure and diverse bioactivities of MDAAs have attracted the attention of researchers. Kuwanon M (KWM) is an MDAA isolated from the root bark of Morus alba. This research reports the growth inhibitory effects of KWM on human lung cancer cells and its possible mechanism. In A549 and NCI-H292 cells, KWM treatment induced suppression of cell proliferation and migration. The appearance of chromatin condensation, phosphatidyl serine exposure and caspase cleavage indicated the arising of apoptosis. The loss of mitochondrial membrane potential (MMP), release of cytochrome c and dysregulation of Bax/Bcl-2 demonstrated that the KWM-induced apoptosis was through the mitochondrial pathway. Paraptosis was simultaneously detected under KWM treatment, as evidenced by the exhibition of cytoplasmic vacuolation, down-regulation of Alix and up-regulation of endoplasmic reticulum (ER) stress-related proteins. Mechanistically, ER stress induced activation of unfolded protein response (UPR) pathways and activation of the MAPK (JNK and ERK) pathway, all of which were critical for KWM-induced apoptosis and paraptosis. These findings suggested the possibility that KWM might be considered as a potential lung cancer therapeutic agent.

show abstract

Section: Resultsmentioning

confidence: 99%

A Mulberry Diels-Alder-Type Adduct, Kuwanon M, Triggers Apoptosis and Paraptosis of Lung Cancer Cells through Inducing Endoplasmic Reticulum Stress

Luan

Zheng

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Mitochondria produce ATP through oxidative phosphorylation, which is necessary for a variety of cellular functions. As mitochondrial metabolism is accompanied by ROS production, the accumulation of damaged mitochondria can activate the mitochondrial apoptotic pathway [31,32] . The mitochondrial apoptotic pathway is one of the main pathways of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Various pro-apoptotic stimuli can decrease mitochondrial membrane potential and increase mitochondrial membrane permeability. These alterations lead to the release of CytC and other pro-apoptotic factors, accelerate apoptotic vesicles formation, and initiate the caspase cascade reaction, eventually leading to apoptosis [31] . SCI often causes mitochondrial damage and is closely associated with apoptosis.…”

Section: Discussionmentioning

confidence: 99%

FUNDC1-Induced Mitophagy Protects Spinal Cord Neurons against Ischemic Injury

Chen

Zhou

Chen

et al. 2023

Preprint

View full text Add to dashboard Cite

Local ischemia and hypoxia are the most important pathological processes in the early phase of secondary spinal cord injury (SCI), in which mitochondria are the main target of ischemic injury. Mitochondrial autophagy, also known as mitophagy, acts as a selective autophagy that specifically identifies and degrades damaged mitochondria, thereby reducing mitochondria-dependent apoptosis. Accumulating evidence shows that the mitophagy receptor, FUN14 domain-containing 1 (FUNDC1), plays an important role in ischemic injury, but the role of FUNDC1 in SCI has not been reported. In this study, we aimed to investigate whether FUNDC1 can enhance mitophagy and inhibit neuronal apoptosis in the early stage of SCI. In a rat SCI model, we found that FUNDC1 overexpression enhanced neuronal autophagy and decreased neuronal apoptosis in the early stage of injury, thereby reducing spinal cord damage. In vitro studies showed that the neuroprotective effects of FUNDC1 were achieved by inhibiting mitochondria-dependent apoptosis and improving mitochondrial function. In addition, FUNDC1 enhanced mitophagy. The protective effects of FUNDC1 against apoptosis and mitochondrial dysfunction were reversed by 3-methyladenine (3-MA), an autophagy inhibitor. Taken together, our results confirm that FUNDC1 can protect against neuronal loss after SCI by inducing mitophagy, inhibiting mitochondria-dependent apoptosis, and improving mitochondrial function.

show abstract

“…Chronic liver disease is caused by viral hepatitis, alcoholic fatty liver disease (AFL), non-alcoholic fatty liver disease (NAFL), drug-induced liver injury (DILI), hepatocellular carcinoma (HCC), and other different etiologies, and the course of disease generally lasts for at least 6 months [ 1 , 2 ]. Some studies have focused on the pathogenesis of chronic liver disease, providing some theoretical support for its prevention and treatment [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction and Chronic Liver Disease

Zhao

Qin

et al. 2022

CIMB

View full text Add to dashboard Cite

Mitochondria are generally considered the powerhouse of the cell, a small subcellular organelle that produces most of the cellular energy in the form of adenosine triphosphate (ATP). In addition, mitochondria are involved in various biological functions, such as biosynthesis, lipid metabolism, oxidative phosphorylation, cell signal transduction, and apoptosis. Mitochondrial dysfunction is manifested in different aspects, like increased mitochondrial reactive oxygen species (ROS), mitochondrial DNA (mtDNA) damage, adenosine triphosphate (ATP) synthesis disorder, abnormal mitophagy, as well as changes in mitochondrial morphology and structure. Mitochondrial dysfunction is related to the occurrence and development of various chronic liver diseases, including hepatocellular carcinoma (HCC), viral hepatitis, drug-induced liver injury (DILI), alcoholic fatty liver (AFL), and non-alcoholic fatty liver (NAFL). In this review, we summarize and discuss the role and mechanisms of mitochondrial dysfunction in chronic liver disease, focusing on and discussing some of the latest studies on mitochondria and chronic liver disease.

show abstract

Mitochondrial Mechanisms of Apoptosis and Necroptosis in Liver Diseases

Cited by 27 publications

References 76 publications

A Mulberry Diels-Alder-Type Adduct, Kuwanon M, Triggers Apoptosis and Paraptosis of Lung Cancer Cells through Inducing Endoplasmic Reticulum Stress

A Mulberry Diels-Alder-Type Adduct, Kuwanon M, Triggers Apoptosis and Paraptosis of Lung Cancer Cells through Inducing Endoplasmic Reticulum Stress

FUNDC1-Induced Mitophagy Protects Spinal Cord Neurons against Ischemic Injury

Mitochondrial Dysfunction and Chronic Liver Disease

Contact Info

Product

Resources

About