Evidence map›Paper›PMID 39789306›Full record

ArticleAmerican journal of hypertension2025

Polo-Like Kinase 2 Ameliorates Lipopolysaccharide-Induced Cardiac Injury by Blocking Cardiomyocyte Ferroptosis.

Bing Xie, Fangfang Li, Jun Yan, Mingyue Cheng, Feng Hui

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Article in American journal of hypertension, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Bing XieDepartment of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Fangfang LiDepartment of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Jun YanDepartment of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Mingyue ChengDepartment of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
Feng HuiDepartment of Cardiology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.ORCID 0009-0009-4273-0128

Funding

National Natural Science Foundation of China 81400178National Natural Science Foundation of China 81900216Natural Science Foundation of Jiangsu Province BK20140226Natural Science Foundation of Jiangsu Province BK20160231Science and Technology Program of Xuzhou KC21067Science and Technology Program of Xuzhou KC21171
6 · The paper itself

Abstract

backgroundPolo-like kinase 2 (PLK2) is associated with cardiac fibrosis in patients with atrial fibrillation. However, the role of PLK2 in sepsis-induced cardiac injury has not been fully elucidated.

methodsWe established a cardiac injury model in C57BL6 mice by injecting lipopolysaccharide (LPS). PLK2 was overexpressed in mice using an adeno-associated virus 9 vector. Cardiac function was evaluated using echocardiography 12 hours after the LPS injection.

resultsMice in the LPS group presented aggravated cardiac injury and a reduced survival rate with increased cardiac inflammatory responses and oxidative stress. Moreover, PLK2 relieved LPS-induced cardiac injury and increased the survival rate of the mice by weakening the inflammatory response and decreasing oxidative stress. Moreover, the LPS-induced increase in ferroptosis was inhibited by PLK2 overexpression. LPS caused an increase in inflammation and cell injury in H9c2 cardiomyocytes, and PLK2 silencing aggravated LPS-induced cell injury, inflammation, and oxidative stress. Furthermore, PLK2 overexpression increased the expression levels of the antiferroptotic proteins solute carrier family 7 member 11, glutathione peroxidase 4, and ferritin in heart tissue. PLK2 increased the nuclear NRF2 expression level. Moreover, the overexpression of PLK2 increased the phosphorylation of glycogen synthase kinase 3β and promoted the nuclear translocation of NRF2. NRF2 overexpression relieved cardiac injury in mice induced with LPS. However, NRF2 mitigated the deteriorating effects of PLK2 knockdown in the mouse heart.

conclusionsPLK2 ameliorated LPS-induced cardiac injury by blocking cardiomyocyte ferroptosis through NRF2 regulation.

Indexed as

FerroptosisMyocytes, CardiacProtein Serine-Threonine KinasesAnimalsCell LineDisease Models, AnimalGlycogen Synthase Kinase 3 betaLipopolysaccharidesMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2Oxidative StressRatsSignal TransductionGlycogen Synthase Kinase 3 betaLipopolysaccharidesNfe2l2 protein, mouseNF-E2-Related Factor 2Protein Serine-Threonine Kinasesblood pressureferroptosishypertensionlipopolysaccharidemiceNRF2polo-like kinase 2sepsis-induced cardiac injury

Identifiers

PMID39789306

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