PFKFB2 Inhibits Ferroptosis in Myocardial Ischemia/Reperfusion Injury Through Adenosine Monophosphate–Activated Protein Kinase Activation

Fu, Caihua; Yu, Shikai; Liu, Zhiquan; Wang, Jiayu; Liu, Ping; Su, Guohai

doi:10.1097/fjc.0000000000001437

Cited by 8 publications

(2 citation statements)

References 34 publications

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“…It has been found that H/R triggers ferroptosis of H9c2 cells [25,78,[103][104][105]. In one study, it was found that deferoxamine inhibited this process [103].…”

Section: Ischemia/reperfusion Of Cardiac Injurymentioning

confidence: 99%

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Ryabov,

Maslov,

Vyshlov

et al. 2024

IJMS

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The hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is about 6% and has not decreased in recent years. The leading cause of death of these patients is ischemia/reperfusion (I/R) cardiac injury. It is quite obvious that there is an urgent need to create new drugs for the treatment of STEMI based on knowledge about the pathogenesis of I/R cardiac injury, in particular, based on knowledge about the molecular mechanism of ferroptosis. In this study, it was demonstrated that ferroptosis is involved in the development of I/R cardiac injury, antitumor drug-induced cardiomyopathy, diabetic cardiomyopathy, septic cardiomyopathy, and inflammation. There is indirect evidence that ferroptosis participates in stress-induced cardiac injury. The activation of AMPK, PKC, ERK1/2, PI3K, and Akt prevents myocardial ferroptosis. The inhibition of HO-1 alleviates myocardial ferroptosis. The roles of GSK-3β and NOS in the regulation of ferroptosis require further study. The stimulation of Nrf2, STAT3 prevents ferroptosis. The activation of TLR4 and NF-κB promotes ferroptosis of cardiomyocytes. MiR-450b-5p and miR-210-3p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation through the inhibition of ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-208a/b, miR-375-3p, miR-26b-5p and miR-15a-5p can aggravate myocardial ferroptosis.

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“…It has been found that H/R triggers ferroptosis of H9c2 cells [25,78,[103][104][105]. In one study, it was found that deferoxamine inhibited this process [103].…”

Section: Ischemia/reperfusion Of Cardiac Injurymentioning

confidence: 99%

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Ryabov,

Maslov,

Vyshlov

et al. 2024

IJMS

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“…Tumor cells increase energy through glycolysis to meet the physiological demands of cell proliferation (Ozcan et al, 2020). 6-phosphofructo-2-kinase/fructose-2,6biphosphatase 2 (PFKFB2) is a regulatory molecule that controls eukaryotic glycolysis (Fu et al, 2023). Studies had found that PFKFB2 overexpression enhanced gastric cancer cell growth and glycolysis (Shen et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

Triptolide restrains the growth, invasion, stemness, and glycolysis of non‐small cell lung cancer cells by PFKFB2‐mediated PI3K/AKT pathway

Ren,

Zhao,

Lai

2024

Chem Biol Drug Des

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Triptolide (TP) has been found to have anti‐tumor effects. However, more potential molecular mechanisms of TP in the progression of non‐small cell lung cancer (NSCLC) deserve further investigation. Cell proliferation, apoptosis, invasion, and stemness were detected by cell counting kit 8 assay, EdU assay, flow cytometry, transwell assay, and sphere formation assay. Cell glycolysis was evaluated by corresponding assay kits. 6‐phosphofructo‐2‐kinase/fructose‐2,6‐biphosphatase 2 (PFKFB2) expression was measured by western blot (WB), qRT‐PCR and immunohistochemical staining. PI3K/AKT pathway‐related markers were determined by WB. Besides, xenograft tumor model was conducted to evaluate the anti‐tumor effect of TP in NSCLC. Our results revealed that TP treatment suppressed NSCLC cell proliferation, invasion, stemness, glycolysis, and enhanced apoptosis. PFKFB2 was upregulated in NSCLC tissues and cells, and its expression was decreased by TP. PFKFB2 knockdown restrained NSCLC cell functions, and its overexpression also eliminated TP‐mediated NSCLC cell functions inhibition. TP decreased PFKFB2 expression to inactivate PI3K/AKT pathway. Moreover, PI3K/AKT pathway inhibitor LY294002 also could reverse the promoting effect of PFKFB2 on NSCLC cell functions. In addition, TP suppressed NSCLC tumorigenesis by inhibiting PFKFB2/PI3K/AKT pathway. In conclusion, TP exerted anti‐tumor role in NSCLC, which was achieved by reducing PFKFB2 expression to inactivate PI3K/AKT pathway.

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Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches

Zhou,

Wang,

Yan

et al. 2024

Cardiovasc Drugs Ther

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PFKFB2 Inhibits Ferroptosis in Myocardial Ischemia/Reperfusion Injury Through Adenosine Monophosphate–Activated Protein Kinase Activation

Cited by 8 publications

References 34 publications

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury

Triptolide restrains the growth, invasion, stemness, and glycolysis of non‐small cell lung cancer cells by PFKFB2‐mediated PI3K/AKT pathway

Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches

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