書誌事項
- タイトル別名
-
- Establishment of a Novel Therapeutic Strategy for Heart Failure Based on the Mechanism Underlying Maintenance of Redox Homeostasis by Reactive Sulfur Species
- Symposium Reviews 活性硫黄種によるレドックス恒常性維持機構に基づいた新規心不全治療戦略の構築
- Symposium Reviews カッセイ イオウシュ ニ ヨル レドックス コウジョウセイ イジ キコウ ニ モトズイタ シンキ シンフゼン チリョウ センリャク ノ コウチク
この論文をさがす
抄録
Cardiac redox homeostasis is precisely regulated by reactive oxygen species (ROS) or electrophilic molecules that are formed by ROS reacting with intracellular substrates, and their eliminating systems. We have focused on the role of nitric oxide (NO) generated from inducible NO synthase (iNOS) that is continuously upregulated from early stage of heart failure, and revealed that iNOS-derived NO acts as a protective factor in the early stage of heart failure, whereas it contributes to induction of cardiac early senescence in later stages. The switching mechanism of NO-mediated signaling includes formation of endogenous NO-derived electrophilic byproducts such as 8-nitroguanosine 3′,5′-cyclic monophosphate (8-nitro-cGMP), which selectively targets an oncogenic small GTPase H-Ras at Cys-184, leading to cardiac cell senescence via covalent modification (S-guanylation) and activation of H-Ras. We also found that hydrogen sulfide-related reactive sulfur species (RSS) function as potent nucleophiles to eliminate electrophilic modification of H-Ras and suppress the onset of chronic heart failure after myocardial infarction. Our results strongly suggest a new concept of redox biology in which suppression of electrophilic irreversible modification of protein cysteine thiols by RSS may be a new therapeutic strategy of cardiovascular diseases.<br>
収録刊行物
-
- 薬学雑誌
-
薬学雑誌 134 (12), 1239-1243, 2014-12-01
公益社団法人 日本薬学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390001206127219456
-
- NII論文ID
- 130004712987
-
- NII書誌ID
- AN00284903
-
- ISSN
- 13475231
- 00316903
-
- NDL書誌ID
- 025939349
-
- PubMed
- 25452233
-
- 本文言語コード
- ja
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
-
- 抄録ライセンスフラグ
- 使用不可