New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases

Riou, Marianne; Alfatni, Abrar; Charles, Anne; Andrès, Emmanuel; Pistea, Cristina; Charloux, Anne; Gény, Bernard

doi:10.3390/jcm9051253

Cited by 11 publications

(8 citation statements)

References 145 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Age-associated chronic obstructive pulmonary disease (COPD) shows many of the hallmarks of aging including impaired autophagy/ mitophagy, accumulation of damaged mitochondria and low grade chronic inflammation (Barnes, 2019). In lung dysfunction, peripheral blood mononuclear cells (PBMCs) and platelets actively participate in inflammation contributing to the severity and lethality of COVID-19 (Riou et al, 2020).…”

Section: Lung Diseasesmentioning

confidence: 99%

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Fernández-Ayala

Navas

López-Lluch

2020

Experimental Gerontology

View full text Add to dashboard Cite

SARS-CoV-2 causes a severe pneumonia (COVID-19) that affects essentially elderly people. In COVID-19, macrophage infiltration into the lung causes a rapid and intense cytokine storm leading finally to a multi-organ failure and death. Comorbidities such as metabolic syndrome, obesity, type 2 diabetes, lung and cardiovascular diseases, all of them age-associated diseases, increase the severity and lethality of COVID-19. Mitochondrial dysfunction is one of the hallmarks of aging and COVID-19 risk factors. Dysfunctional mitochondria is associated with defective immunological response to viral infections and chronic inflammation. This review discuss how mitochondrial dysfunction is associated with defective immune response in aging and different age-related diseases, and with many of the comorbidities associated with poor prognosis in the progression of COVID-19. We suggest here that chronic inflammation caused by mitochondrial dysfunction is responsible of the explosive release of inflammatory cytokines causing severe pneumonia, multi-organ failure and finally death in COVID-19 patients. Preventive treatments based on therapies improving mitochondrial turnover, dynamics and activity would be essential to protect against COVID-19 severity.

show abstract

Section: Lung Diseasesmentioning

confidence: 99%

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Fernández-Ayala

Navas

López-Lluch

2020

Experimental Gerontology

View full text Add to dashboard Cite

show abstract

“…Mitochondrial dysfunction and its potential mechanistic role in the pathophysiology of lung diseases such as COPD, asthma, pulmonary arterial hypertension, or idiopathic pulmonary fibrosis is increasingly recognised (9)(10)(11). Clinical observational data suggest that mitochondrial dysfunction has been associated with higher mortality in critically ill patients with sepsis (12) and survivors of the Multiple Organ Dysfunction Syndrome had better mitochondrial function with preservation of ATP and biogenesis markers (13).…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal stromal cell extracellular vesicles rescue mitochondrial dysfunction and improve barrier integrity in clinically relevant models of ARDS

et al. 2020

View full text Add to dashboard Cite

Alveolar epithelial-capillary barrier disruption is a hallmark of Acute Respiratory Distress Syndrome (ARDS). Contribution of mitochondrial dysfunction to the compromised alveolar-capillary barrier in ARDS remains unclear. Mesenchymal stromal cells-derived extracellular vesicles (MSC EVs) are considered as a cell free therapy for ARDS. Mitochondrial transfer was shown to be important for the therapeutic effects of MSCs and MSC EVs. Here we investigated the contribution of mitochondrial dysfunction to the injury of alveolar epithelial and endothelial barriers in ARDS and the ability of MSC EVs to modulate alveolar-capillary barrier integrity through mitochondrial transfer.Primary human small airway epithelial and pulmonary microvascular endothelial cells and human precision cut lung slices (PCLSs) were stimulated with endotoxin or plasma samples from patients with ARDS and treated with MSC EVs, barrier properties and mitochondrial functions were evaluated. LPS-injured mice were treated with MSC EVs and degree of lung injury and mitochondrial respiration of the lung tissue were assessed.Inflammatory stimulation resulted in increased permeability coupled with pronounced mitochondrial dysfunction in both types of primary cells and PCLSs. EVs derived from normal MSCs restored barrier integrity and normal levels of oxidative phosphorylation while EV preparation which did not contain mitochondria was not effective. In vivo, presence of mitochondria was critical for EV ability to reduce lung injury and restore mitochondrial respiration in the lung tissue.In the ARDS environment MSC-EVs improve alveolar-capillary barrier properties through restoration of mitochondrial functions at least partially via mitochondrial transfer.

show abstract

“…Nevertheless, most HF patients, whether with a reduced or preserved EF, have multiple comorbidities, and future studies trying to control comorbidities might be an important way to tease out the specific effects of these comorbidities, as they may produce differential molecular pathways to achieve the same vicious cycle of inflammation. Accordingly, individuals with a normal cardiac function but with type II diabetes, asthma exacerbation or pulmonary hypertension presented with an increased PBMC mitochondrial function [55][56][57].…”

Section: Conclusion and Current Challengesmentioning

confidence: 99%

Pathophysiology of Heart Failure: A Role for Peripheral Blood Mononuclear Cells Mitochondrial Dysfunction?

Sauer

Riou

Charles

et al. 2022

JCM

Self Cite

View full text Add to dashboard Cite

Heart failure (HF) is a leading cause of hospitalization in patients aged more than 65 years and is associated with high mortality rates. A better comprehension of its physiopathology is still needed, and, in addition to neurohormonal systems and sodium glucose co-transporter 2 modulations, recent studies focus on the mitochondrial respiration of peripheral blood circulating cells (PBMCs). Thus, cardiovascular metabolic risk factors and cellular switch with an increased neutrophil/lymphocytes ratio might favor the decreased PBMC mitochondrial respiration observed in relation with HF severity. PBMCs are implicated in the immune system function and mitochondrial dysfunction of PBMC, potentially induced by their passage through a damaged heart and by circulating mitoDAMPs, which can lead to a vicious circle, thus sustaining negative cardiac remodeling during HF. This new approach of HF complex pathophysiology appears to be a promising field of research, and further studies on acute and chronic HF with reduced or preserved LVEF are warranted to better understand whether circulating PBMC mitochondrial function and mitoDAMPs follow-ups in HF patients might show diagnosis, prognosis or therapeutic usefulness.

show abstract

New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases

Cited by 11 publications

References 145 publications

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Age-related mitochondrial dysfunction as a key factor in COVID-19 disease

Mesenchymal stromal cell extracellular vesicles rescue mitochondrial dysfunction and improve barrier integrity in clinically relevant models of ARDS

Pathophysiology of Heart Failure: A Role for Peripheral Blood Mononuclear Cells Mitochondrial Dysfunction?

Contact Info

Product

Resources

About