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Purpose: This study examines the protective effects of fenofibrate on retinal health in diabetic retinopathy, focusing on its ability to reduce inflammation, oxidative stress, and restore autophagy while preventing ferroptosis.
Methods: Using a streptozotocin (STZ)-induced diabetic rat model and cultured ARPE-19 cells under high glucose conditions, we assessed the impact of fenofibrate on oxidative stress markers, autophagy-related proteins, and tight junction integrity. Fenofibrate's role in modulating inflammation and preventing ferroptosis was also evaluated.
Results: Fenofibrate treatment reduced ROS production and NADPH oxidase activity, alleviating oxidative stress in retinal tissues. Additionally, fenofibrate enhanced autophagy, as indicated by increased LC3 expression, and maintained tight junction protein expression. These effects contributed to the stabilization of cellular homeostasis, potentially slowing disease progression.
Conclusion: Fenofibrate offers significant protective effects in diabetic retinopathy by reducing inflammation and oxidative stress, promoting autophagy, and inhibiting ferroptosis, making it a promising therapeutic option for managing the disease.
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http://dx.doi.org/10.1080/02713683.2025.2516802 | DOI Listing |
Plant Dis
September 2025
Shenyang Agricultural University, College of Plant Protection, Nematology Institute of Northern China, Shenyang, China;
Root-knot nematodes (Meloidogyne spp.) cause catastrophic yield losses in global agriculture. This study identified itaconic acid (IA), through comparative metabolomic analysis (the study of small molecules in biological systems), as a key virulence-related metabolite produced by the fungus Trichoderma citrinoviride Snef1910.
View Article and Find Full Text PDFAnim Sci J
January 2025
Department of Animal Science, Bangladesh Agricultural University, Mymensingh, Bangladesh.
This study investigates the effects of L-carnitine on nuclear maturation and fertilization in cattle and goat oocytes. Ovaries were collected from females with poor reproductive efficiency in the tropical climate, and cumulus-oocyte complexes (COCs) were retrieved from large antral follicles. COCs were cultured with varying concentrations of L-carnitine (0, 0.
View Article and Find Full Text PDFCell Commun Signal
September 2025
Department of Cytology, Institute of Anatomy, Medical Faculty, Ruhr-University Bochum, Universitätsstr. 150, Building MA 5/52, Bochum, 44801, Germany.
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.
Nature
September 2025
Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Monocyte-derived macrophages (mo-macs) often drive immunosuppression in the tumour microenvironment (TME) and tumour-enhanced myelopoiesis in the bone marrow fuels these populations. Here we performed paired transcriptome and chromatin accessibility analysis over the continuum of myeloid progenitors, circulating monocytes and tumour-infiltrating mo-macs in mice and in patients with lung cancer to identify myeloid progenitor programs that fuel pro-tumorigenic mo-macs. We show that lung tumours prime accessibility for Nfe2l2 (NRF2) in bone marrow myeloid progenitors as a cytoprotective response to oxidative stress, enhancing myelopoiesis while dampening interferon response and promoting immunosuppression.
View Article and Find Full Text PDFNature
September 2025
Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA.
Loss-of-function variants in the lipid transporter ABCA7 substantially increase the risk of Alzheimer's disease, yet how they impact cellular states to drive disease remains unclear. Here, using single-nucleus RNA-sequencing analysis of human brain samples, we identified widespread gene expression changes across multiple neural cell types associated with rare ABCA7 loss-of-function variants. Excitatory neurons, which expressed the highest levels of ABCA7, showed disrupted lipid metabolism, mitochondrial function, DNA repair and synaptic signalling pathways.
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