The Role of Arachidonic Acid Metabolism in Myocardial Ischemia–Reperfusion Injury

Zhang, Changjiang; He, Miao; Ni, Lihua; He, Ke; Su, Ke; Deng, Yinzhi; Li, Yuanhong; Xia, Hao

doi:10.1007/s12013-020-00928-z

Cited by 29 publications

(25 citation statements)

References 81 publications

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“…By binding to 4G protein-coupled receptors, PGE2, the downstream proinflammatory product of AA, could enable the activation of adenylate cyclase as well as numerous downstream signaling pathways, thereby promoting the expression levels of many inflammatory factors, such as TNF-α, IL-1, and IL-6. 37 Chen et al reported that, compared with the healthy control, in serum samples of CHD-PAH, α-linolenic acid metabolism and AA metabolism were remarkably disturbed. 25 Consistently, in the present study, linoleic acid metabolism and AA metabolism pathways have been proven to be the most pivotal dysregulated pathways in PAs and the RV, evidenced by high impact values obtained in KEGG pathway analysis based on the selected 39 shared differential PA and RV metabolites.…”

Section: Discussionmentioning

confidence: 99%

“…AA, synthesized from linoleic acid, is a long-chain fatty acid that could be converted into LTs by lipoxygenase or into PGH2 by COXs. By binding to 4G protein-coupled receptors, PGE2, the downstream proinflammatory product of AA, could enable the activation of adenylate cyclase as well as numerous downstream signaling pathways, thereby promoting the expression levels of many inflammatory factors, such as TNF-α, IL-1, and IL-6 . Chen et al reported that, compared with the healthy control, in serum samples of CHD-PAH, α-linolenic acid metabolism and AA metabolism were remarkably disturbed .…”

Section: Discussionmentioning

confidence: 99%

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Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model

Liu

Qin

et al. 2021

ACS Omega

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Pulmonary arterial hypertension (PAH) is a complex devastating disease relevant to remarkable metabolic dysregulation. Although various research studies on PAH from a metabolic perspective have been emerging, pathogenesis of PAH varies in different categories. Research on metabolic reprogramming in flow-associated PAH remains insufficient. An untargeted metabolomic profiling platform was used to evaluate the metabolic profile of pulmonary arteries (PAs) as well as the right ventricle (RV) in a flow-associated PAH rat model in the present work. A total of 79 PAs and 128 RV metabolites were significantly altered in PAH rats, among which 39 metabolites were assessed as shared dysregulated metabolites in PAs and the RV. Pathway analysis elucidated that, in PAs of PAH rats, pathways of phenylalanine, tyrosine, and tryptophan biosynthesis and linoleic acid metabolism were significantly altered, while in the RV, arginine biosynthesis and linoleic acid metabolism were altered dramatically. Further integrated analysis of shared dysregulated PA and RV metabolites demonstrated that the linoleic acid metabolism and the arachidonic acid (AA) metabolism were the key pathways involved in the pathogenesis of flow-associated PAH. Results obtained from the present work indicate that the PAH pathogenesis could be mediated by widespread metabolic reprogramming. In particular, the dysregulation of AA metabolism may considerably contribute to the development of high blood flow-associated PAH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model

Liu

Qin

et al. 2021

ACS Omega

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“…Tissue plasminogen activator (tPA) and tPA recombinant protein were both used to treat ischemic stroke. However, these treatments have dangerous complications regarding reperfusion-injury ( 173 ). Reperfusion-injury generally causes oxidative stress, calcium overload and excitatory toxicity ( 174 ).…”

Section: Drugs That Target Mitochondriamentioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1β release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.

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“…MIRI mechanism involves several processes, including energy metabolism disorder, oxidative stress, calcium overload, inflammation, apoptosis and autophagy (33). In the clinic, the best treatment for patients with myocardial infarction is immediate reperfusion, causing a paradoxical situation because of its adverse effects (34).…”

Section: Discussionmentioning

confidence: 99%

DL‑3‑n‑butylphthalide protects H9c2 cardiomyoblasts from ischemia/reperfusion injury by regulating HSP70 expression via PI3K/AKT pathway activation

Zhu

Sun

et al. 2021

Exp Ther Med

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DL-3-n-butylphthalide (NBP) is commonly used to treat ischemic strokes due to its antioxidative and anti-inflammatory effects. The present study aimed to examine the protective effects of NBP on myocardial ischemia-reperfusion injury (MIRI) by establishing a MIRI model in H9c2 cells. Cell viability assay using Cell Counting Kit-8, lactate dehydrogenase (LDH) cytotoxicity and lipid peroxidation malondialdehyde (MDA) content were assessed to detect cell activity, degree of cell injury and oxidative stress reaction. Reverse transcription-quantitative PCR was used to quantify the expression of inflammatory factors in H9c2 cells. Western blotting and immunofluorescence staining were used to detect the protein expression of PI3K/AKT and heat shock protein 70 (HSP70). The present results indicated that NBP significantly increased cell viability during ischemia-reperfusion. Moreover, NBP inhibited the release of LDH and the production of MDA. NBP treatment also significantly decreased the expression of inflammatory factors at the mRNA level. Additionally, NBP activated the PI3K/AKT pathway and upregulated the expression of HSP70 compared with cells in the MIRI model. LY294002, a PI3K inhibitor, reversed the protective effects of NBP and suppressed the expression of HSP70. The present study demonstrated that NBP protected H9c2 cells from MIRI by regulating HSP70 expression via PI3K/AKT pathway activation.

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The Role of Arachidonic Acid Metabolism in Myocardial Ischemia–Reperfusion Injury

Cited by 29 publications

References 81 publications

Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model

Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

DL‑3‑n‑butylphthalide protects H9c2 cardiomyoblasts from ischemia/reperfusion injury by regulating HSP70 expression via PI3K/AKT pathway activation

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