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Background: Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by oxidative stress and progressive motor neuron degeneration. This study evaluates the potential neuroprotective effects of caffeine in the Wobbler mouse, an established model of ALS.

Methods: Wobbler mice received caffeine supplementation (60 mg/kg/day) via drinking water, and key parameters, including muscle strength, NAD metabolism, oxidative stress, and motor neuron morphology, were assessed at critical disease stages.

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Methodology and evaluation of the induction of experimental autoimmune encephalomyelitis, a murine preclinical model of multiple sclerosis.

Methods Cell Biol

September 2025

Instituto de Biomedicina y Genética Molecular de Valladolid (IBGM-CSIC/UVA), Valladolid, Spain. Electronic address:

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that is characterized by a severe and progressive demyelinating process. It is considered a neurodegenerative autoimmune disorder driven by immune cell infiltration, overproduction of cytokines and reactive oxygen species (ROS) accumulation that leads to axonal and neuronal injury. Experimental autoimmune encephalomyelitis (EAE) is the most commonly used pre-clinical model of multiple sclerosis (MS), since it resembles many aspects of the human disease.

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Background: Electronic nicotine delivery systems (ENDS) utilize "E-liquids" in order to generate "E-vapor", an inhalable aerosolized mixture containing nicotine and flavors. Flavored ENDS are very popular among teens who vape, however, the possible cardiac electrophysiological harm of inhalation exposure to flavored ENDS are not fully understood.

Objective: To test if inhalation exposure to flavoring carbonyls in e-liquids compromises mitochondrial integrity, increases oxidative stress, and leads to cardiac electrophysiological toxicity.

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Hypertriglyceridemia impairs HDL functionality, promotes macrophage metabolic activation and exacerbates antigen-induced rheumatoid arthritis in mice which can be reversed by fenofibrate treatment.

Biochim Biophys Acta Mol Cell Biol Lipids

September 2025

Laboratory of Biochemistry, University of Crete Medical School and Gene Regulation and Genomics group, Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology of Hellas, Heraklion, Crete, Greece. Electronic address:

Rheumatoid arthritis (RA) is associated with increased cardiovascular disease (CVD) risk, partly attributed to altered lipid metabolism. Apolipoprotein C-III (apoC-III), a key regulator of triglyceride-rich lipoproteins in the plasma, has been implicated in both dyslipidemia and inflammation. In this study, we investigated the role of hypertriglyceridemia in RA using a transgenic mouse model overexpressing the human apoC-III gene (apoC-III Tg).

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Senolytic therapy increases replicative capacity by eliminating senescent endothelial cells.

Exp Gerontol

September 2025

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA; Salk Institute for Biological Studies, La Jolla, CA, 92037, USA; Department of Molecular Biology, University of Utah, Salt Lake City, UT, USA; Department of Biochemistry, University of Utah, Salt Lake Ci

Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression.

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