Mitochondrial quality control: from molecule to organelle

Roca-Portoles, Alba; Tait, Stephen W.G.

doi:10.1007/s00018-021-03775-0

Cited by 85 publications

(65 citation statements)

References 187 publications

(274 reference statements)

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“…Importantly, clearance of such mitochondria should be both swift and efficient to eliminate the possibility of cancer cell persistence and propagation. Fundamental to ensuring only 'healthy' and fully functioning mitochondria exist within the cell are a range of quality control measures such as mitophagy and mito-nuclear communication to ensure the damaged, exhausted or sub-optimal mitochondrial are eliminated or repaired (expertly reviewed: [178]).…”

Section: Metabolism and Therapy Resistance: Exploiting Imposed Vulnerabilities To Improve Responsementioning

confidence: 99%

Metabolic Reprogramming: A Friend or Foe to Cancer Therapy?

McCann¹,

Kerr²

2021

Cancers

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Drug resistance is a major cause of cancer treatment failure, effectively driven by processes that promote escape from therapy-induced cell death. The mechanisms driving evasion of apoptosis have been widely studied across multiple cancer types, and have facilitated new and exciting therapeutic discoveries with the potential to improve cancer patient care. However, an increasing understanding of the crosstalk between cancer hallmarks has highlighted the complexity of the mechanisms of drug resistance, co-opting pathways outside of the canonical “cell death” machinery to facilitate cell survival in the face of cytotoxic stress. Rewiring of cellular metabolism is vital to drive and support increased proliferative demands in cancer cells, and recent discoveries in the field of cancer metabolism have uncovered a novel role for these programs in facilitating drug resistance. As a key organelle in both metabolic and apoptotic homeostasis, the mitochondria are at the forefront of these mechanisms of resistance, coordinating crosstalk in the event of cellular stress, and promoting cellular survival. Importantly, the appreciation of this role metabolism plays in the cytotoxic response to therapy, and the ability to profile metabolic adaptions in response to treatment, has encouraged new avenues of investigation into the potential of exploiting metabolic addictions to improve therapeutic efficacy and overcome drug resistance in cancer. Here, we review the role cancer metabolism can play in mediating drug resistance, and the exciting opportunities presented by imposed metabolic vulnerabilities.

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Section: Metabolism and Therapy Resistance: Exploiting Imposed Vulnerabilities To Improve Responsementioning

confidence: 99%

Metabolic Reprogramming: A Friend or Foe to Cancer Therapy?

McCann¹,

Kerr²

2021

Cancers

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“…Mitochondria remain in a stable state by the number of mitochondria and their form and/or function changing to meet the high demands of cellular bioenergetics and stress response pathways. In mammalian cells, damaged mitochondria are specifically identified and removed via autophagy (mitophagy) in a highly context-dependent manner that spares healthy organelle process known as “mitochondrial quality control” [ 19 – 21 ]. New mitochondria can be synthesized, and a healthy and functional mitochondrial population is thus maintained.…”

Section: Mitochondrial Quality Controlmentioning

confidence: 99%

Mitochondrial Mechanisms of Apoptosis and Necroptosis in Liver Diseases

Chu

Zheng

et al. 2021

Analytical Cellular Pathology

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In addition to playing a pivotal role in cellular energetics and biosynthesis, mitochondrial components are key operators in the regulation of cell death. In addition to apoptosis, necrosis is a highly relevant form of programmed liver cell death. Differential activation of specific forms of programmed cell death may not only affect the outcome of liver disease but may also provide new opportunities for therapeutic intervention. This review describes the role of mitochondria in cell death and the mechanism that leads to chronic liver hepatitis and liver cirrhosis. We focus on mitochondrial-driven apoptosis and current knowledge of necroptosis and discuss therapeutic strategies for targeting mitochondrial-mediated cell death in liver diseases.

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“…Therefore, these organelles are subject to finely regulated MQC mechanisms, which respond to stress stimuli and activate a network of pathways that act dynamically to maintain a highly efficient population of mitochondria [5]. MQC mechanisms include (i) mitochondrial biogenesis, which involves the expansion of mitochondrial numbers; (ii) mitochondrial dynamics (fusion and fission), which allows the redistribution and exchange of mitochondrial components among the mitochondrial population; (iii) mitochondrial autophagy (mitophagy), related to the selective degradation of mitochondria; and (iv) mitochondria-controlled cell death (Figure 2) [48,49].…”

Section: Mitochondrial Quality Control In Cardioprotectionmentioning

confidence: 99%

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

García-Niño

Zazueta

Buelna‐Chontal

et al. 2021

Life

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Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction.

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Mitochondrial quality control: from molecule to organelle

Cited by 85 publications

References 187 publications

Metabolic Reprogramming: A Friend or Foe to Cancer Therapy?

Metabolic Reprogramming: A Friend or Foe to Cancer Therapy?

Mitochondrial Mechanisms of Apoptosis and Necroptosis in Liver Diseases

Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury

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