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

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

Material type
記事
Author
Shen Xiaoyuほか
Publisher
International Heart Journal Association
Publication date
2024-05-31
Material Format
Digital
Journal name
International Heart Journal 65 3
Publication Page
p.537-547
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Detailed bibliographic record

Summary, etc.:

<p>Cardiomyocyte lipotoxicity and ferroptosis are the key to the development of diabetic cardiomyopathy (DCM). Perilipin 5 (PLIN5) is perceived as a s...

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Digital

Material Type
記事
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
Target Audience
一般
Standard No. (Other)
PMID : 38749744
References
Pyrin Inflammasome Regulates Tight Junction Integrity to Restrict Colitis and Tumorigenesis
Inflammasomes in neuroinflammatory and neurodegenerative diseases
Plin5, a New Target in Diabetic Cardiomyopathy
Copper-dependent autophagic degradation of GPX4 drives ferroptosis
Effects of Sodium/Glucose Cotransporter 2 (SGLT2) Inhibitors on Cardiovascular and Metabolic Outcomes in Patients Without Diabetes Mellitus: A Systematic Review and Meta‐Analysis of Randomized‐Controlled Trials
Role of Dapagliflozin and Liraglutide on Diabetes-Induced Cardiomyopathy in Rats: Implication of Oxidative Stress, Inflammation, and Apoptosis
Electroacupuncture inhibits the interaction between peripheral TRPV1 and P2X3 in rats with different pathological pain
Ferroptosis as a novel therapeutic target for cardiovascular disease
Role of Oxidative Stress in Metabolic and Subcellular Abnormalities in Diabetic Cardiomyopathy
Perilipin5 protects against lipotoxicity and alleviates endoplasmic reticulum stress in pancreatic β-cells
The role of cardiac lipotoxicity in the pathogenesis of diabetic cardiomyopathy
Basal PIR expression in HeLa cells is driven by NRF2 via evolutionary conserved antioxidant response element
Ferroptosis and its potential role in the physiopathology of Parkinson’s Disease
Cardiac Energy Metabolism in Heart Failure
Hepatic PLIN5 signals via SIRT1 to promote autophagy and prevent inflammation during fasting
Mir-675-5p supports hypoxia-induced drug resistance in colorectal cancer cells
TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway
Diabetic cardiomyopathy - A comprehensive updated review
Inhibition of ferroptosis by up-regulating Nrf2 delayed the progression of diabetic nephropathy
Perilipin5 protects against non-alcoholic steatohepatitis by increasing 11-Dodecenoic acid and inhibiting the occurrence of ferroptosis
What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review
Iron accumulation and lipid peroxidation: implication of ferroptosis in diabetic cardiomyopathy
Evogliptin, a DPP-4 inhibitor, prevents diabetic cardiomyopathy by alleviating cardiac lipotoxicity in db/db mice
Lipotoxicity-induced mtDNA release promotes diabetic cardiomyopathy by activating the cGAS-STING pathway in obesity-related diabetes
Heart failure in patients with type 2 diabetes mellitus: assessment with echocardiography and effects of antihyperglycemic treatments
Canagliflozin Attenuates Lipotoxicity in Cardiomyocytes by Inhibiting Inflammation and Ferroptosis through Activating AMPK Pathway
Ferroptosis is essential for diabetic cardiomyopathy and is prevented by sulforaphane via AMPK/NRF2 pathways
Inhibition of Nrf2/HO-1 signaling leads to increased activation of the NLRP3 inflammasome in osteoarthritis
Pirin is an iron-dependent redox regulator of NF-κB
Broadening horizons: the role of ferroptosis in cancer
Low cardiac lipolysis reduces mitochondrial fission and prevents lipotoxic heart dysfunction in Perilipin 5 mutant mice
Corydalis saxicola Bunting total alkaloids attenuate paclitaxel-induced peripheral neuropathy through PKCε/p38 MAPK/TRPV1 signaling pathway
Curcumin decreases epithelial‑mesenchymal transition by a Pirin‑dependent mechanism in cervical cancer cells
Canagliflozin mitigates ferroptosis and improves myocardial oxidative stress in mice with diabetic cardiomyopathy
MiR-93-5p promotes granulosa cell apoptosis and ferroptosis by the NF-kB signaling pathway in polycystic ovary syndrome
Mitochondrial damage and activation of the cytosolic DNA sensor cGAS–STING pathway lead to cardiac pyroptosis and hypertrophy in diabetic cardiomyopathy mice
NOX4 promotes ferroptosis of astrocytes by oxidative stress-induced lipid peroxidation via the impairment of mitochondrial metabolism in Alzheimer's diseases
Role of Pirin, an Oxidative Stress Sensor Protein, in Epithelial Carcinogenesis
Pirin: A novel redox-sensitive modulator of primary and secondary metabolism in Streptomyces
Mitophagy Is Essential for Maintaining Cardiac Function During High Fat Diet-Induced Diabetic Cardiomyopathy
Muscle Lipid Metabolism: Role of Lipid Droplets and Perilipins
Mechanisms of diabetic cardiomyopathy and potential therapeutic strategies: preclinical and clinical evidence
Data Provider (Database)
国立情報学研究所 : CiNii Research

Digital

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
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インターネット公開
Data Provider (Database)
科学技術振興機構 : J-STAGE