The mitochondrial membrane potential (ΔΨ ) is a parameter often used to determine mitochondrial function; therefore, it can be used to determine the integrity and functionality of cells. A decrement of ΔΨ is implicated in several inflammatory-related pathologies, such phenomena can be related to COVID-19 infection. The present work aimed to compare the ΔΨ in leucocytes (human PBMCs; HPBMC) isolated from healthy control (HC) subjects, patients with COVID-19 (C-19), recovered subjects at 40 ± 13 (R1) and 335 ± 20 (R2) days after infection (dai). Obtained data showed that ΔΨ decreased in HPBMC of subjects with C-19, R1, and R2 compared with HC. When analyzing the ΔΨ data by sex, in females, a significant decrease was observed in R1 and R2 groups versus HC. Regarding men, a significant decrease of ΔΨ was observed in R1, with respect to HC, contrary to R2 group, who reestablished this parameter. Obtained results suggest that the loss of ΔΨ could be related to the long-COVID.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9088601PMC
http://dx.doi.org/10.1002/JLB.3MA0322-279RRRDOI Listing

Publication Analysis

Top Keywords

mitochondrial membrane
8
membrane potential
8
ΔΨ
8
potential ΔΨ
8
ΔΨ leucocytes
8
loss mitochondrial
4
leucocytes post-covid-19
4
post-covid-19 sequelae
4
sequelae mitochondrial
4
ΔΨ parameter
4

Similar Publications

Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a rare neurodegenerative disorder characterized by spastic paraplegia, parkinsonism and psychiatric and/or behavioral symptoms caused by variants in gene encoding chromosome-19 open reading frame-12 (C19orf12). We present here seven patients from six unrelated families with detailed clinical, radiological, and genetic investigations. Childhood-onset patients predominantly had a spastic ataxic phenotype with optic atrophy, while adult-onset patients were presented with cognitive, behavioral, and parkinsonian symptoms.

View Article and Find Full Text PDF

Long non-coding RNA XR008038 promotes the myocardial ischemia/reperfusion injury development through increasing the expressions of galectin-3.

Int J Cardiol

January 2025

Department of Intensive Care Unit, Hangzhou Hospital of Traditional Chinese Medicine (Dingqiao District), Guangxing Affiliated Hospital of Zhejiang Chinese Medical University, No.453 Tiyuchang Road, Hangzhou, Zhejiang 310013, China. Electronic address:

Background: Myocardial ischemia/reperfusion (I/R) injury is a common pathophysiological change after myocardial reperfusion therapy. Recent research confirmed that long non-coding RNA (IncRNAs) played an important role in many cardiovascular diseases. This study was carried out to explore the role of lncRNA XR008038 in the I/R progression.

View Article and Find Full Text PDF

Pulmonary fibrosis (PF) arises from dysregulated wound healing, leading to excessive extracellular matrix (ECM) deposition and impaired lung function. Macrophages exhibit high plasticity, polarizing to pro-inflammatory M1 during early inflammation and anti-inflammatory, fibrosis-inducing M2 during later stages of PF. Additionally, neutrophils and neutrophil extracellular traps (NETs) release mediated by peptidyl arginine deiminase (PAD-4), also play a key role in PF progression.

View Article and Find Full Text PDF

A non-purine inhibitor of xanthine oxidoreductase mitigates adenosine triphosphate degradation under hypoxic conditions in mouse brain.

Brain Res

January 2025

Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo, Japan. Electronic address:

The brain is an organ that consumes a substantial amount of oxygen, and a reduction in oxygen concentration can rapidly lead to significant and irreversible brain injury. The progression of brain injury during hypoxia involves the depletion of intracellular adenosine triphosphate (ATP) due to decreased oxidative phosphorylation in the inner mitochondrial membrane. Allopurinol is a purine analog inhibitor of xanthine oxidoreductase that protects against hypoxic/ischemic brain injury; however, its underlying mechanism of action remains unclear.

View Article and Find Full Text PDF

Elevating VAPB-PTPIP51 integration repairs damaged mitochondria-associated endoplasmic reticulum membranes and inhibits lung fibroblasts activation.

Int Immunopharmacol

January 2025

School of Public Health, the key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang, Guizhou, 561113, China. Electronic address:

Long-term silica exposure to silica dust leads to irreversible pulmonary fibrosis, during which lung fibroblast activation plays an essential role. Mitochondria-associated endoplasmic reticulum membranes (MAMs) is a structural interface for communication between the outer mitochondrial membrane and the endoplasmic reticulum. VAPB-PTPIP51 is a key complex on MAMs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!