Mitochondrial Dysfunction as a Hallmark of Environmental Injury

Duarte-Hospital, Carolina; Tête, Arnaud; Brial, François; Benoit, Louise; Koual, Meriem; Tomkiewicz, Céline; Kim, Min Ji; Blanc, Étienne; Coumoul, Xavier; Bortoli, Sylvie

doi:10.3390/cells11010110

Cited by 42 publications

(24 citation statements)

References 90 publications

(103 reference statements)

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“…Exposure to external stimuli, such as multiple environmental contaminants, affects the normal structure and function of the mitochondria, leading to metabolic and functional diseases [ 21 , 22 ]. Recent studies have provided insights into the involvement of mitochondrial function defects that are induced by the toxicity of environmental contaminants [ 23 , 24 , 25 ] ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

Impact of Micro- and Nanoplastics on Mitochondria

Lee

Moon

et al. 2022

Metabolites

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Mitochondria are highly dynamic cellular organelles that perform crucial functions such as respiration, energy production, metabolism, and cell fate decisions. Mitochondrial damage and dysfunction critically lead to the pathogenesis of various diseases including cancer, diabetes, and neurodegenerative and cardiovascular disorders. Mitochondrial damage in response to environmental contaminant exposure and its association with the pathogenesis of diseases has also been reported. Recently, persistent pollutants, such as micro- and nanoplastics, have become growing global environmental threats with potential health risks. In this review, we discuss the impact of micro- and nanoplastics on mitochondria and review current knowledge in this field.

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Section: Introductionmentioning

confidence: 99%

Impact of Micro- and Nanoplastics on Mitochondria

Lee

Moon

et al. 2022

Metabolites

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“…Maintaining the cellular mitochondrial health is mediated via different processes such as mitochondrial fission, fusion, biogenesis, and mitophagy [ 39 ]. Early studies have shown that an imbalance in the cellular energy demand due to environmental stress can alter the different mitochondrial processes and thus can adversely affect the overall mitochondrial quality [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury

Sivakumar

Alasmari

Ali

et al. 2022

Biology

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A previous study has reported that exposure to PM2.5 from diesel exhaust (diesel particulate matter (DPM)) for 21 days can deteriorate the cardiac recovery from myocardial ischemia reperfusion injury (IR), where the latter is facilitated by the efficiency of mitochondrial subpopulations. Many investigators have demonstrated that IR impact on cardiac mitochondrial subpopulations is distinct. In the present study, we decipher the role of PM2.5 on IR associated mitochondrial dysfunction at the subpopulation level by administrating PM2.5 directly to isolated female rat hearts via KH buffer. Our results demonstrated that PM2.5 administered heart (PM_C) severely deteriorated ETC enzyme activity (NQR, SQR, QCR, and COX) and ATP level in both IFM and SSM from the normal control. Comparatively, the declined activity was prominent in IFM fraction. Moreover, in the presence of IR (PM_IR), mitochondrial oxidative stress was higher in both subpopulations from the normal, where the IFM fraction of mitochondria experienced elevated oxidative stress than SSM. Furthermore, we assessed the in vitro protein translation capacity of IFM and SSM and found a declined ability in both subpopulations where the inability of IFM was significant in both PM_C and PM_IR groups. In support of these results, the expression of mitochondrial genes involved in fission, fusion, and mitophagy events along with the DNA maintenance genes such as GUF1, LRPPRC, and HSD17-b10 were significantly altered from the control. Based on the above results, we conclude that PM2.5 administration to the heart inflicted mitochondrial damage especially to the IFM fraction, that not only deteriorated the cardiac physiology but also reduced its ability to resist IR injury.

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“…Mounting evidence has shown that AhR is involved in the regulation of cellular metabolism in many types of cells by acting as a TF to control the expression of metabolism-related genes, by interacting with intracellular signaling pathways related to metabolism, or by disturbing mitochondrial function 56, 57 . AhR is expressed by various immune cells, and its signaling exerts integrative effects on the cellular environment and metabolism of the immune responses 58 .…”

Section: Discussionmentioning

confidence: 99%

Uremic toxin indoxyl sulfate induces trained immunityviathe AhR-dependent arachidonic acid pathway in end-stage renal disease (ESRD)

Kim

Lee

et al. 2022

Preprint

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Trained immunity is the long-term functional reprogramming of innate immune cells following exposure to various insults that results in altered responses towards a secondary challenge. Indoxyl sulfate (IS) is a potent uremic stimulus associated with inflammation in chronic kidney disease (CKD). However, the impact of IS on trained immunity remains unknown. Here, we find that IS induces trained immunity in monocytes via epigenetic and metabolic reprogramming, resulting in augmented cytokine production upon LPS-stimulation. Further, the aryl hydrocarbon receptor contributes to IS-trained immunity by enhancing expression of arachidonic acid metabolism-related genes ALOX5 and ALOX5AP. Monocytes from end-stage renal disease (ESRD) patients have increased ALOX5 expression and healthy monocytes trained with uremic sera from ESRD patients exhibit increased TNF-α and IL-6 production. Moreover, IS-trained mice have augmented TNF-α production following LPS-stimulation. These results provide insight into the role of IS in trained immunity, which is critical during inflammatory responses in CKD patients.

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Mitochondrial Dysfunction as a Hallmark of Environmental Injury

Cited by 42 publications

References 90 publications

Impact of Micro- and Nanoplastics on Mitochondria

Impact of Micro- and Nanoplastics on Mitochondria

Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury

Uremic toxin indoxyl sulfate induces trained immunityviathe AhR-dependent arachidonic acid pathway in end-stage renal disease (ESRD)

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