Mitochondria as Targets for Endothelial Protection in COVID-19

Попова, Е. Н.; Zinovkina, L. A.; Lyamzaev, Konstantin G.; Zinovkin, Roman A.

doi:10.3389/fphys.2020.606170

Cited by 8 publications

(6 citation statements)

References 37 publications

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“…It is not difficult to find an abiotic, a substance that kills all living things, while the search for antibiotics, substances that kill bacteria and do not kill eukaryotic cells, is a difficult task. Among the most promising antibacterial agents are mitochondria-targeted antioxidants, which can effectively kill bacterial cells, cure damaged host cells, and reduce hypercytokinemia [ 1 , 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Observation of Cytotoxicity of Phosphonium Derivatives Is Explained: Metabolism Inhibition and Adhesion Alteration

et al. 2023

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The search for new antibiotics, substances that kill prokaryotic cells and do not kill eukaryotic cells, is an urgent need for modern medicine. Among the most promising are derivatives of triphenylphosphonium, which can protect the infected organs of mammals and heal damaged cells as mitochondria-targeted antioxidants. In addition to the antioxidant action, triphenylphosphonium derivatives exhibit antibacterial activity. It has recently been reported that triphenylphosphonium derivatives cause either cytotoxic effects or inhibition of cellular metabolism at submicromolar concentrations. In this work, we analyzed the MTT data using microscopy and compared them with data on changes in the luminescence of bacteria. We have shown that, at submicromolar concentrations, only metabolism is inhibited, while an increase in alkyltriphenylphosphonium (CnTPP) concentration leads to adhesion alteration. Thus, our data on eukaryotic and prokaryotic cells confirm a decrease in the metabolic activity of cells by CnTPPs but do not confirm a cytocidal effect of TPPs at submicromolar concentrations. This allows us to consider CnTPP as a non-toxic antibacterial drug at low concentrations and a relatively safe vector for delivering other antibacterial substances into bacterial cells.

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Section: Introductionmentioning

confidence: 99%

Observation of Cytotoxicity of Phosphonium Derivatives Is Explained: Metabolism Inhibition and Adhesion Alteration

et al. 2023

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“…Thus, the infection of endothelial cells by SARS-COV-2 might contribute to mitochondrial dysfunction and oxidative stress, key players on the initiation of chronic inflammation and endothelial damage 71 . Drugs targeting mitochondria and/or some of the proteins highlighted here could be considered as potential tools for protecting the endothelium in severe forms of COVID-19 72 .…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular-related proteomic changes in ECFCs exposed to the serum of COVID-19 patients

Beltrán-Camacho¹,

Bhosale²,

Sánchez-Morillo³

et al. 2023

Int. J. Biol. Sci.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection significantly affects the cardiovascular system, causing vascular damage and thromboembolic events in critical patients. Endothelial dysfunction represents one of the first steps in response to COVID-19 that might lead to cardiovascular complications and long-term sequelae. However, despite the enormous efforts in the last two years, the molecular mechanisms involved in such processes remain poorly understood. Herein, we analyzed the protein changes taking place in endothelial colony forming cells (ECFCs) after the incubation with the serum from individuals infected with COVID-19, whether asymptomatic or critical patients, by application of a label free-quantitative proteomics approach. Specifically, ECFCs from healthy individuals were incubated ex-vivo with the serum of either COVID-19 negative donors (PCR-/IgG-, n:8), COVID-19 asymptomatic donors at different infective stages (PCR+/ IgG-, n:8and PCR-/IgG+, n:8), or hospitalized critical COVID-19 patients (n:8), followed by proteomics analysis. In total, 590 proteins were differentially expressed in ECFCs in response to all infected serums. Predictive analysis highlighted several proteins like CAPN5, SURF4, LAMP2 or MT-ND1, as highly discriminating features between the groups compared. Protein changes correlated with viral infection, RNA metabolism or autophagy, among others. Remarkably, the angiogenic potential of ECFCs in response to the infected serums was impaired, and many of the protein alterations in response to the serum of critical patients were associated with cardiovascular-related pathologies.

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“…Although studies of asymptomatic infected individuals are lacking, the immunological profiles of patients with moderate infections indicate a protective T cell-dependent response, in contrast to patients with severe disease who exhibit an exacerbated systemic inflammation, with signs of T cells exhaustion [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Role of Immunometabolism and Mitochondrial Health in Inflammaging and Fight against Viral Diseases

2022

JCEI

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Mitochondria as Targets for Endothelial Protection in COVID-19

Cited by 8 publications

References 37 publications

Observation of Cytotoxicity of Phosphonium Derivatives Is Explained: Metabolism Inhibition and Adhesion Alteration

Observation of Cytotoxicity of Phosphonium Derivatives Is Explained: Metabolism Inhibition and Adhesion Alteration

Cardiovascular-related proteomic changes in ECFCs exposed to the serum of COVID-19 patients

Role of Immunometabolism and Mitochondrial Health in Inflammaging and Fight against Viral Diseases

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