Mitochondria Related Cell Death Modalities and Disease

Tian, Chuwen; Liu, Yifan; Li, Zhuoshu; Zhu, Ping; Zhao, Mingyi

doi:10.3389/fcell.2022.832356

Cited by 56 publications

(30 citation statements)

References 235 publications

(235 reference statements)

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“…Mitochodria play important roles in cellular energy metabolism and cell survival, and a key role in adenosine triphosphate generation through oxidative phosphorylation 19 . Mitochondria can not only generate adenosine triphosphate, but also control various types of cell death, such as apoptosis, pyroptosis, necroptosis and ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

Increased oxidative stress caused by impaired mitophagy aggravated liver ischemia and reperfusion injury in diabetic mice

Kong

Zhang

et al. 2022

J of Diabetes Invest

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Aims/Introduction Emerging evidence has suggested the detrimental role of oxidative stress in aggravating ischemia and reperfusion (IR) injury in diabetic livers. Interplay between oxidative stress and mitophagy has been shown. However, the role and mechanism of mitophagy in regulating oxidative stress and IR injury in diabetic livers remain unclear. Materials and Methods Wild‐type and db / db (DB) mice were subjected to a partial warm liver IR model. Liver injury, oxidative stress, mitophagy and related molecular pathways were analyzed. Results Here, we found that increased liver IR injury was observed in DB mice, as evidenced by higher levels of serum alanine aminotransferase and serum aspartate, worsened liver architecture damage and more hepatocellular death. DB mice also showed increased mitochondrial oxidative stress. Mitochondrial reactive oxygen species scavenge alleviated liver IR injury in DB mice. Mechanistic analysis showed that 5′ adenosine monophosphate‐activated protein kinase‐mediated mitophagy was suppressed in DB mice post‐IR. Pharmacological activation of 5′ adenosine monophosphate‐activated protein kinase by its agonist effectively restored mitophagy activation, leading to decreased mitochondrial oxidative stress and attenuated liver IR injury in DB mice. Conclusions Our findings showed that diabetes increased oxidative stress to exacerbate liver IR injury by impairing 5′ adenosine monophosphate‐activated protein kinase‐mediated mitophagy. Strategies targeting oxidative stress and mitophagy might provide a promising approach to ameliorate liver IR injury in diabetes patients.

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Section: Discussionmentioning

confidence: 99%

Increased oxidative stress caused by impaired mitophagy aggravated liver ischemia and reperfusion injury in diabetic mice

Kong

Zhang

et al. 2022

J of Diabetes Invest

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“…This way, uncontrolled cell proliferation results in the development of diseases such as cancer or RA, while an excessive level of cell death can lead to diseases such as Alzheimer’s or Parkinson’s [ 182 ]. Mitochondria also have a central position in regulating cell death [ 182 , 183 ]. As a result, it is not conspicuous that damaged mitochondria have been associated to multiple acute and chronic diseases as RA [ 184 ].…”

Section: Mitochondrial Oxidative Stress and Cell Death In Ramentioning

confidence: 99%

“…Interestingly, caspase-1 is able to initiate apoptosis [ 137 ], highlighting the interplay between cell death and inflammasome activation [ 194 ]. As commented above, the intrinsic pathway is associated to mitochondria and is inducible by multiple stimuli, including high levels of mtROS [ 183 , 195 ]; these produce the activation of BH3 proteins that, in turn, activate BAX and BAK, triggering the permeabilization of the mitochondrial outer membrane [ 194 ]. In fact, the crucial event of intrinsic apoptosis is the mitochondrial outer membrane permeabilization, which leads to the liberate of cytochrome c and the assembling of the prominent complex apoptosome [ 196 , 197 ]; that subsequently causes the downstream cascade activation.…”

Section: Mitochondrial Oxidative Stress and Cell Death In Ramentioning

confidence: 99%

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Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis

2022

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Control of excessive mitochondrial oxidative stress could provide new targets for both preventive and therapeutic interventions in the treatment of chronic inflammation or any pathology that develops under an inflammatory scenario, such as rheumatoid arthritis (RA). Increasing evidence has demonstrated the role of mitochondrial alterations in autoimmune diseases mainly due to the interplay between metabolism and innate immunity, but also in the modulation of inflammatory response of resident cells, such as synoviocytes. Thus, mitochondrial dysfunction derived from several danger signals could activate tricarboxylic acid (TCA) disruption, thereby favoring a vicious cycle of oxidative/mitochondrial stress. Mitochondrial dysfunction can act through modulating innate immunity via redox-sensitive inflammatory pathways or direct activation of the inflammasome. Besides, mitochondria also have a central role in regulating cell death, which is deeply altered in RA. Additionally, multiple evidence suggests that pathological processes in RA can be shaped by epigenetic mechanisms and that in turn, mitochondria are involved in epigenetic regulation. Finally, we will discuss about the involvement of some dietary components in the onset and progression of RA.

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“…The core function of mitochondria is energy generation for maintaining tissue homeostasis and conduits for programmed apoptosis requires strict control the quality and quantity of mitochondria [ 8 , 42 ]. Disturbances in mitochondrial homeostasis can lead to cell death, leading to a range of metabolic disorders [ 43 ]. Mitophagy uses lysosomes to selectively remove dysfunctional or damaged mitochondria, maintaining mitochondrial quality [ 44 ].…”

Section: Mitochondria-mediated Inflammationmentioning

confidence: 99%

Mitochondrial Control in Inflammatory Gastrointestinal Diseases

Sui

Wang

Liu

et al. 2022

IJMS

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Mitochondria play a central role in the pathophysiology of inflammatory bowel disease (IBD) and colorectal cancer (CRC). The maintenance of mitochondrial function is necessary for a stable immune system. Mitochondrial dysfunction in the gastrointestinal system leads to the excessive activation of multiple inflammatory signaling pathways, leading to IBD and increased severity of CRC. In this review, we focus on the mitochondria and inflammatory signaling pathways and its related gastrointestinal diseases.

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Mitochondria Related Cell Death Modalities and Disease

Cited by 56 publications

References 235 publications

Increased oxidative stress caused by impaired mitophagy aggravated liver ischemia and reperfusion injury in diabetic mice

Increased oxidative stress caused by impaired mitophagy aggravated liver ischemia and reperfusion injury in diabetic mice

Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis

Mitochondrial Control in Inflammatory Gastrointestinal Diseases

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