دورية أكاديمية

PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis.

التفاصيل البيبلوغرافية
العنوان: PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis.
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
الوصف
تدمد:1349-3299
DOI:10.1536/ihj.24-002