دورية أكاديمية
PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis.
العنوان: | PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis. |
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المؤلفون: | Shen X; Department of Endocrinology, Shanghai TCM-Integrated Hospital., Zhang J; Department of Cardiovascular Medicine, Shanghai TCM-Integrated Hospital., Zhou Z; Department of Cardiovascular Medicine, Shanghai TCM-Integrated Hospital., Yu R; Department of Cardiovascular Medicine, Shanghai TCM-Integrated Hospital. |
المصدر: | International heart journal [Int Heart J] 2024 May 31; Vol. 65 (3), pp. 537-547. Date of Electronic Publication: 2024 May 15. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: International Heart Journal Association Country of Publication: Japan NLM ID: 101244240 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1349-3299 (Electronic) Linking ISSN: 13492365 NLM ISO Abbreviation: Int Heart J Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: [Tokyo, Japan] : International Heart Journal Association, [2005]- |
مواضيع طبية MeSH: | Ferroptosis* , Myocytes, Cardiac*/metabolism , Myocytes, Cardiac*/pathology , Perilipin-5*/metabolism , Diabetic Cardiomyopathies*/metabolism , NF-kappa B*/metabolism, Animals ; Mice ; Reactive Oxygen Species/metabolism ; Cell Survival ; Palmitic Acid/pharmacology ; Signal Transduction |
مستخلص: | Cardiomyocyte lipotoxicity and ferroptosis are the key to the development of diabetic cardiomyopathy (DCM). Perilipin 5 (PLIN5) is perceived as a significant target of DCM. This study aimed to focus on the role and mechanism of PLIN5 on lipotoxicity and ferroptosis in DCM.Following transfection, mouse cardiomyocytes HL-1 were induced by 0.1 mM palmitic acid (PA) to set up lipotoxic cardiomyocyte models. The cell viability and lipid accumulation were evaluated by cell counting kit-8 assay and Oil red O staining, respectively. Ferrous ion (Fe 2+ ), glutathione (GSH), malondialdehyde (MDA), and reactive oxygen species (ROS) levels were determined to verify the effects of PLIN5 or Pirin (PIR) on ferroptosis. Quantitative real-time reverse transcription polymerase chain reaction or Western blot was performed for quantitative analysis.PLIN5 overexpression promoted the viability, GSH level, and expression of GPX4/PIR/intracellular P65, yet suppressed lipid accumulation, level of Fe 2+ /MDA/ROS, and expression of interleukin (IL)-1β/IL-18/intranuclear P65 in PA-stimulated HL-1 cells. PIR silencing counteracted the roles of PLIN5 overexpression in PA-stimulated HL-1 cells.PLIN5 suppresses lipotoxicity and ferroptosis in cardiomyocyte via modulating PIR/NF-κB axis, hinting its potential as a therapeutic target in DCM. |
فهرسة مساهمة: | Keywords: Cardiomyocyte lipotoxicity; Cell death; Diabetic cardiomyopathy; Inflammation; Iron metabolism; NF-κB pathway |
المشرفين على المادة: | 0 (Perilipin-5) 0 (NF-kappa B) 0 (Plin5 protein, mouse) 0 (Reactive Oxygen Species) 2V16EO95H1 (Palmitic Acid) |
تواريخ الأحداث: | Date Created: 20240515 Date Completed: 20240602 Latest Revision: 20240602 |
رمز التحديث: | 20240603 |
DOI: | 10.1536/ihj.24-002 |
PMID: | 38749744 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1349-3299 |
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DOI: | 10.1536/ihj.24-002 |