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| http://dx.doi.org/10.1007/s13312-021-2180-z | DOI Listing |
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Preparation, structural property, and antioxidant activities of a novel pectin polysaccharide from the flowers of Linn.
Front Nutr
January 2025
Prefabricated Dish Industry Development Research Institute, Zhejiang Dong Fang Polytechnic, Wenzhou, China.
Introduction: Oxidative stress, triggered by an imbalance between reactive oxygen species (ROS) production and cellular antioxidant defense mechanisms, is implicated in various pathological conditions. Plant-derived polysaccharides have gained significant attention as potential natural antioxidants due to their biocompatibility, biodegradability, and structural versatility.
Methods: This study focuses on the purification, structural characterization, and antioxidant activities of a novel pectin polysaccharide (HFPS) isolated from the flowers of Linn.
Methyltransferase-like 3 mediates m6A modification of heme oxygenase 1 mRNA to induce ferroptosis of renal tubular epithelial cells in acute kidney injury.
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Traditional Chinese Medicine Integrated Department of Nephrology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; Research Institute of Nephrology, Zhengzhou University, Zhengzhou, Henan province, China; Henan Province Research Center for Kidney Disease, Zhengzhou, Henan Province, China; Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, Zhengzhou, Henan Province, China; Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, China; Innovation Center of Basic Research for Metabolic-Associated Fatty Liver Disease, Ministry of Education of China, Zhengzhou, Henan Province, China. Electronic address:
Acute kidney injury (AKI) involves a series of syndromes characterized by a rapid increase in creatinine levels. Ferroptosis, as an iron-dependent mode of programmed cell death, reportedly participates in the pathogenesis of AKI. Methyltransferase-like 3 (METTL3)-mediated m6A modification has been recently associated with various kidney diseases; however, the mechanism of METTL3 crosstalk with the molecules involved in ferroptosis is not clearly understood.
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