The role of ferroptotic cell death-related HMGB1 in inflammation crosstalk with cancer and myocardial Ischemia/reperfusion injury
dc.authorscopusid | 55515395600 | |
dc.authorscopusid | 6602873428 | |
dc.authorscopusid | 36543258600 | |
dc.contributor.author | Kaya, Salih Tunç | |
dc.contributor.author | Güven, Celal | |
dc.contributor.author | Taşkın, E. | |
dc.date.accessioned | 2023-07-26T11:57:32Z | |
dc.date.available | 2023-07-26T11:57:32Z | |
dc.date.issued | 2022 | |
dc.department | DÜ, Fen-Edebiyat Fakültesi, Biyoloji Bölümü | en_US |
dc.description.abstract | Inflammation is one of the critical defense pathways against pathogen and pathologic conditions, including cancer and myocardial ischemia/ reperfusion (MIR) injury. Therefore, inflammation has positive and negative impacts on tissues and organs. There are two types of inflammation, named as acute and chronic inflammation. The inflammation is also involved in the development of cancer and myocardial infarction. Damage-associated molecular patterns (DAMPs), such as High Mobility Group Box-1 (HMGB1), heat shock proteins (HSPs), ATP, and S100 proteins, are conservative danger molecules released from damaged or dying cells to trigger an immune response. However, they have essential roles in pathological inflammation to participate in self-defense in physiological and pathological circumstances. Recent evidence has emerged that inflammation may be a significant factor in the development and/or progression of cancer and myocardial infarction. Herein, we review current research on the role of HMGB1 in cancer and myocardial ischemia/reperfusion injury, focusing on inflammation. Furthermore, we have discussed the role of the posttranslational modification of HMGB1 in both illnesses. In addition, we focus on a new cell death pathway named ferroptosis, which may be involved in the development of both cancer and MIR through inflammation by HMGB1. © 2023 by Nova Science Publishers, Inc. All rights reserved. | en_US |
dc.identifier.endpage | 74 | en_US |
dc.identifier.isbn | 9798886974669 | |
dc.identifier.isbn | 9798886974089 | |
dc.identifier.scopus | 2-s2.0-85143993339 | en_US |
dc.identifier.startpage | 43 | en_US |
dc.identifier.uri | https://hdl.handle.net/20.500.12684/13218 | |
dc.indekslendigikaynak | Scopus | en_US |
dc.institutionauthor | Kaya, Salih Tunç | |
dc.language.iso | en | en_US |
dc.publisher | Nova Science Publishers, Inc. | en_US |
dc.relation.ispartof | HMGB1: Functions, Inhibitors and Clinical Significance | en_US |
dc.relation.publicationcategory | Kitap Bölümü - Uluslararası | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.snmz | $2023V1Guncelleme$ | en_US |
dc.subject | Cancer | en_US |
dc.subject | Ferroptosis | en_US |
dc.subject | High mobility group box-1 | en_US |
dc.subject | Inflammation | en_US |
dc.subject | Myocardial ischemia/reperfusion injury | en_US |
dc.subject | Posttranslational modification | en_US |
dc.title | The role of ferroptotic cell death-related HMGB1 in inflammation crosstalk with cancer and myocardial Ischemia/reperfusion injury | en_US |
dc.type | Book Chapter | en_US |