Unravelling the Connection Between Energy Metabolism and Immune Senescence/Exhaustion in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Biomolecules, Год журнала: 2025, Номер 15(3), С. 357 - 357

Опубликована: Март 1, 2025

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease, characterized by diverse array of symptoms including post-exertional malaise (PEM), severe fatigue, and cognitive impairments, all which drastically diminish the patients’ quality life. Despite its impact, no curative treatments exist, largely due to limited understanding disease’s underlying pathophysiology. Mitochondrial dysfunction, leading impaired energy production utilization, believed play key role in onset fatigue PEM, positioning it as potential pathophysiological mechanism ME/CFS. Additionally, disorder shows similarities chronic viral infections, with frequent reports immune system alterations, suggesting critical for (dys)functioning. In particular, roles senescence exhaustion—two fundamental states—remain poorly understood This state-of-the-art review explores how metabolic dysfunction may be interconnected ME/CFS, proposing that deficits directly impair function. By examining this metabolic–immune interplay, highlights pathways developing innovative therapeutic strategies target both metabolism regulation, offering hope improving patient outcomes.

Язык: Английский

Umbilical mesenchymal stem cells mitigate T-cell compartments shift and Th17/Treg imbalance in acute ischemic stroke via mitochondrial transfer

Stem Cell Research & Therapy, Год журнала: 2025, Номер 16(1)

Опубликована: Март 12, 2025

Acute ischemic stroke (AIS) initiates secondary injuries that worsen neurological damage and hinder recovery. While peripheral immune responses play a key role in outcomes, clinical results from immunotherapy have been suboptimal, with limited focus on T-cell dynamics. Umbilical mesenchymal stem cells (UMSCs) offer therapeutic potential due to their immunomodulatory properties. They can regulate reduce neuroinflammation, potentially enhancing recovery by fostering pro-regenerative environment. However, the effect of UMSCs dynamics AIS remains underexplored. This study investigates following examines how may mitigate dysregulation develop better treatment strategies. patients (NIHSS scores 0–15) were recruited within 72 h onset, blood samples collected Day 0 (enrollment) 7. compartments identified flow cytometry, plasma cytokine levels quantified using cytometric bead array (CBA). Mitochondria labeled MitoTracker. Peripheral mononuclear isolated, treated lipopolysaccharide (LPS), cocultured both direct contact Transwell systems. Flow CBA, RT-qPCR, immunofluorescence assays used detect compartments, gene expression markers for helper T (Th) cell differentiation, profiles, mitochondrial transfer, reactive oxygen species (ROS) production, membrane potential. Additionally, DNA was depleted. The effects mitochondria-depleted mice compared through behavioral assessments analysis microenvironment. In AIS, underwent phenotypic shift naïve effector or memory states, specific increase Th17 decrease regulatory cells, leading alterations T-cell-mediated functions. an ex vivo co-culture system, LPS stimulation further amplified these disparities, inducing dysfunction oxidative stress cells. Notably, restored function reversed transfer. Critically, UMSC significantly improved deficits disorders mice, whereas failed produce this effect. Our comprehensive insights into attributes acute mechanisms provide crucial theoretical foundation understanding treatment.

Язык: Английский

Mitochondrial Dynamics Regulators in Cancer Metabolism and Progression

Mitochondrial Communications, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский