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      Progress of medicinal plants and their active metabolites in ischemia-reperfusion injury of stroke: a novel therapeutic strategy based on regulation of crosstalk between mitophagy and ferroptosis

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          Abstract

          The death of cells can occur through various pathways, including apoptosis, necroptosis, mitophagy, pyroptosis, endoplasmic reticulum stress, oxidative stress, ferroptosis, cuproptosis, and disulfide-driven necrosis. Increasing evidence suggests that mitophagy and ferroptosis play crucial regulatory roles in the development of stroke. In recent years, the incidence of stroke has been gradually increasing, posing a significant threat to human health. Hemorrhagic stroke accounts for only 15% of all strokes, while ischemic stroke is the predominant type, representing 85% of all stroke cases. Ischemic stroke refers to a clinical syndrome characterized by local ischemic-hypoxic necrosis of brain tissue due to various cerebrovascular disorders, leading to rapid onset of corresponding neurological deficits. Currently, specific therapeutic approaches targeting the pathophysiological mechanisms of ischemic brain tissue injury mainly include intravenous thrombolysis and endovascular intervention. Despite some clinical efficacy, these approaches inevitably lead to ischemia-reperfusion injury. Therefore, exploration of treatment options for ischemic stroke remains a challenging task. In light of this background, advancements in targeted therapy for cerebrovascular diseases through mitophagy and ferroptosis offer a new direction for the treatment of such diseases. In this review, we summarize the progress of mitophagy and ferroptosis in regulating ischemia-reperfusion injury in stroke and emphasize their potential molecular mechanisms in the pathogenesis. Importantly, we systematically elucidate the role of medicinal plants and their active metabolites in targeting mitophagy and ferroptosis in ischemia-reperfusion injury in stroke, providing new insights and perspectives for the clinical development of therapeutic drugs for these diseases.

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          Regulation of ferroptotic cancer cell death by GPX4.

          Wan Seok Yang, Rohitha SriRamaratnam, Matthew E Welsch … (2014)
          Ferroptosis is a form of nonapoptotic cell death for which key regulators remain unknown. We sought a common mediator for the lethality of 12 ferroptosis-inducing small molecules. We used targeted metabolomic profiling to discover that depletion of glutathione causes inactivation of glutathione peroxidases (GPXs) in response to one class of compounds and a chemoproteomics strategy to discover that GPX4 is directly inhibited by a second class of compounds. GPX4 overexpression and knockdown modulated the lethality of 12 ferroptosis inducers, but not of 11 compounds with other lethal mechanisms. In addition, two representative ferroptosis inducers prevented tumor growth in xenograft mouse tumor models. Sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPX4-regulated ferroptosis. Thus, GPX4 is an essential regulator of ferroptotic cancer cell death. Copyright © 2014 Elsevier Inc. All rights reserved.
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            Ferroptosis: molecular mechanisms and health implications

            Daolin Tang, Xin CHEN, Rui Kang … (2020)
            Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012, there has been mounting interest in the process and function of ferroptosis. Ferroptosis can occur through two major pathways, the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants, which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products. Accordingly, ferroptosis is precisely regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional and posttranslational layers. The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense, whereas selective autophagy may promote ferroptotic death. Here, we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection.
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              Lipid peroxidation and ferroptosis: The role of GSH and GPx4.

              Fulvio Ursini, Matilde Maiorino (2020)
              Ferroptosis (FPT) is a form of cell death due to missed control of membrane lipid peroxidation (LPO). According to the axiomatic definition of non-accidental cell death, LPO takes place in a scenario of altered homeostasis. FPT, differently from apoptosis, occurs in the absence of any known specific genetically encoded death pathway or specific agonist, and thus must be rated as a regulated, although not "programmed", death pathway. It follows that LPO is under a homeostatic metabolic control and is only permitted when indispensable constraints are satisfied and the antiperoxidant machinery collapses. The activity of the selenoperoxidase Glutathione Peroxidase 4 (GPx4) is the cornerstone of the antiperoxidant defence. Converging evidence on both mechanism of LPO and GPx4 enzymology indicates that LPO is initiated by alkoxyl radicals produced by ferrous iron from the hydroperoxide derivatives of lipids (LOOH), traces of which are the unavoidable drawback of aerobic metabolism. FPT takes place when a threshold has been exceeded. This occurs when the major conditions are satisfied: i) oxygen metabolism leading to the continuous formation of traces of LOOH from phospholipid-containing polyunsaturated fatty acids; ii) missed enzymatic reduction of LOOH; iii) availability of ferrous iron from the labile iron pool. Although the effectors impacting on homeostasis and leading to FPT in physiological conditions are not known, from the available knowledge on LPO and GPx4 enzymology we propose that it is aerobic life itself that, while supporting bioenergetics, is also a critical requisite of FPT. Yet, when the homeostatic control of the steady state between LOOH formation and reduction is lost, LPO is activated and FPT is executed.
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                Author and article information

                Contributors
                Guozhen Zhang: Role: Role:
                Qiang Wang: Role: Role: Role:
                Bing Jiang: Role: Role: Role:
                Lihe Yao: Role: Role: Role:
                Wenjuan Wu: Role: Role: Role:
                Xiaoyan Zhang: Role: Role:
                Dongjun Wan: Role: Role:
                Youquan Gu: URI : https://loop.frontiersin.org/people/2636639/overviewRole: Role: Role:
                Journal
                Journal ID (nlm-ta): Front Pharmacol
                Journal ID (iso-abbrev): Front Pharmacol
                Journal ID (publisher-id): Front. Pharmacol.
                Title: Frontiers in Pharmacology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-9812
                Publication date (Electronic): 08 April 2024
                Publication date Collection: 2024
                Volume: 15
                Electronic Location Identifier: 1374445
                Affiliations
                [1] 1 College of the First Clinical Medicine , Lanzhou University , Lanzhou, Gansu, China
                [2] 2 Department of Neurology , People’s Liberation Army Joint Logistics Support Force 940th Hospital , Lanzhou, Gansu, China
                [3] 3 Department of Neurology , First Hospital of Lanzhou University , Lanzhou, Gansu, China
                [4] 4 Department of Integrated Chinese and Western Medicine , Gansu University of Traditional Chinese Medicine , Lanzhou, Gansu, China
                Author notes

                Edited by: Stalin Antony, University of Electronic Science and Technology of China, China

                Reviewed by: Bin-Nan Wu, Kaohsiung Medical University, Taiwan

                Amro M. Soliman, University of Alberta, Canada

                *Correspondence: Youquan Gu, guyq940@ 123456163.com
                Article
                Publisher ID: 1374445
                DOI: 10.3389/fphar.2024.1374445
                PMC ID: 11033413
                PubMed ID: 38650626
                SO-VID: 0232adbe-4e4a-400d-9199-a96aaab6ab2e
                Copyright © Copyright © 2024 Zhang, Wang, Jiang, Yao, Wu, Zhang, Wan and Gu.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 22 January 2024
                Date accepted : 25 March 2024
                Funding
                The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by The Fund of The First Hospital of Lanzhou University (No. ldyyyn2020-108); Natural Science Foundation of Gansu Province (No. 20JR10RA671).
                Categories
                Subject: Pharmacology
                Subject: Review
                Custom metadata
                section-at-acceptance Ethnopharmacology

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: mitophagy,ferroptosis,ischemia-reperfusion injury in stroke,medicinal plants,active metabolites
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: mitophagy, ferroptosis, ischemia-reperfusion injury in stroke, medicinal plants, active metabolites

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