PLIN5 Suppresses Lipotoxicity and Ferroptosis in Cardiomyocyte via Modulating PIR/NF-κB Axis
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- Material Type
- 記事
- Author Heading
- Publication Date
- 2024-05-31
- Publication Date (W3CDTF)
- 2024-05-31
- Periodical title
- International Heart Journal
- No. or year of volume/issue
- 65 3
- Volume
- 65
- Issue
- 3
- Pages
- 537-547
- Publication date of volume/issue (W3CDTF)
- 2024-05-31
- ISSN (Periodical Title)
- 13492365
- ISSN-L (Periodical Title)
- 13492365
- Publication (Periodical Title)
- International Heart Journal Association
- Text Language Code
- en
- Subject Heading
- Target Audience
- 一般
- Standard No. (Other)
- PMID : 38749744
- DOI
- 10.1536/ihj.24-002
- Related Material (URI)
- References
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- 国立情報学研究所 : CiNii Research
- Original Data Provider (Database)
- Japan Link CenterCrossrefPubMed
- Summary, etc.
- <p>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.</p><p>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<sup>2+</sup>), 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.</p><p>PLIN5 overexpression promoted the viability, GSH level, and expression of GPX4/PIR/intracellular P65, yet suppressed lipid accumulation, level of Fe<sup>2+</sup>/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.</p><p>PLIN5 suppresses lipotoxicity and ferroptosis in cardiomyocyte via modulating PIR/NF-κB axis, hinting its potential as a therapeutic target in DCM.</p>
- DOI
- 10.1536/ihj.24-002
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 科学技術振興機構 : J-STAGE