Generation of Reactive Oxygen Species by Mitochondria

Hernansanz-Agustín, Pablo; Enrı́quez, José Antonio

doi:10.3390/antiox10030415

Cited by 208 publications

(135 citation statements)

References 121 publications

Supporting

Mentioning

112

Contrasting

Order By: Relevance

“…Mitochondrial dynamics require the recruitment of proteins to mitochondria. Indeed, the importation of several proteins to mitochondria depends on proton electrochemical gradient H + created by ETS at the IMM, which is called the proton motive force (PMF) [157]. In addition, several redox-sensitive proteins are activated to induce proteins translocation from the cytosol.…”

Section: Redox-sensitive Proteins Participating In Fission and Fusionmentioning

confidence: 99%

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

et al. 2021

View full text Add to dashboard Cite

Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

show abstract

Section: Redox-sensitive Proteins Participating In Fission and Fusionmentioning

confidence: 99%

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

et al. 2021

View full text Add to dashboard Cite

show abstract

“…mtNOS is considered the main source of RNS [118]. Mitochondrial complexes I (CI) and III (CIII) are the major sources of ROS within the mitochondria and the cell [119]. Mitochondria that produce ROS may generate oxidized phospholipids and isoprostanes, affecting inflammation and cancer progression.…”

Section: Mitochondrial Activitymentioning

confidence: 99%

Effects of Dietary n–3 and n–6 Polyunsaturated Fatty Acids in Inflammation and Cancerogenesis

Liput

Lepczyński

Ogłuszka

et al. 2021

IJMS

139

View full text Add to dashboard Cite

The dietary recommendation encourages reducing saturated fatty acids (SFA) in diet and replacing them with polyunsaturated fatty acids (PUFAs) n–3 (omega–3) and n–6 (omega–6) to decrease the risk of metabolic disturbances. Consequently, excessive n–6 PUFAs content and high n–6/n–3 ratio are found in Western-type diet. The importance of a dietary n–6/n–3 ratio to prevent chronic diseases is linked with anti-inflammatory functions of linolenic acid (ALA, 18:3n–3) and longer-chain n–3 PUFAs. Thus, this review provides an overview of the role of oxylipins derived from n–3 PUFAs and oxylipins formed from n–6 PUFAs on inflammation. Evidence of PUFAs’ role in carcinogenesis was also discussed. In vitro studies, animal cancer models and epidemiological studies demonstrate that these two PUFA groups have different effects on the cell growth, proliferation and progression of neoplastic lesions.

show abstract

“…With disruptions in OXPHOS being touted as a major contributor to ROS production [ 127 ], POLG patient-derived iPSC-NSCs and iPSC-DANs showed increased ROS levels that could be improved following N-acetylcysteine amide supplementation [ 125 , 126 ]. An increase in ROS was otherwise not detected in the patient iPSCs, while patient fibroblasts showed reduced ROS levels instead when compared to controls [ 125 ].…”

Section: Functional Studiesmentioning

confidence: 99%

Modelling Mitochondrial Disease in Human Pluripotent Stem Cells: What Have We Learned?

McKnight

Low

Elliott

et al. 2021

IJMS

View full text Add to dashboard Cite

Mitochondrial diseases disrupt cellular energy production and are among the most complex group of inherited genetic disorders. Affecting approximately 1 in 5000 live births, they are both clinically and genetically heterogeneous, and can be highly tissue specific, but most often affect cell types with high energy demands in the brain, heart, and kidneys. There are currently no clinically validated treatment options available, despite several agents showing therapeutic promise. However, modelling these disorders is challenging as many non-human models of mitochondrial disease do not completely recapitulate human phenotypes for known disease genes. Additionally, access to disease-relevant cell or tissue types from patients is often limited. To overcome these difficulties, many groups have turned to human pluripotent stem cells (hPSCs) to model mitochondrial disease for both nuclear-DNA (nDNA) and mitochondrial-DNA (mtDNA) contexts. Leveraging the capacity of hPSCs to differentiate into clinically relevant cell types, these models permit both detailed investigation of cellular pathomechanisms and validation of promising treatment options. Here we catalogue hPSC models of mitochondrial disease that have been generated to date, summarise approaches and key outcomes of phenotypic profiling using these models, and discuss key criteria to guide future investigations using hPSC models of mitochondrial disease.

show abstract

Generation of Reactive Oxygen Species by Mitochondria

Cited by 208 publications

References 121 publications

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

Effects of Dietary n–3 and n–6 Polyunsaturated Fatty Acids in Inflammation and Cancerogenesis

Modelling Mitochondrial Disease in Human Pluripotent Stem Cells: What Have We Learned?

Contact Info

Product

Resources

About