| Japanese |
|---|
| Title | 全身性炎症反応症候群における活性酸素種の病態修飾機構 |
|---|
| Subtitle | 特集 |
|---|
| Authors | 松田直之 |
|---|
| Authors(kana) | |
|---|
| Organization | 京都大学大学院医学研究科初期診療・救急医学分野 |
|---|
| Journal | 循環制御 |
|---|
| Volume | 30 |
|---|
| Number | 2 |
|---|
| Page | 72-81 |
|---|
| Year/Month | 2009/12 |
|---|
| Article | 報告 |
|---|
| Publisher | 日本循環制御医学会 |
|---|
| Abstract | 『はじめに』 活性酸素種(ROS：reactive oxygen species)の存在が分子レベルで報告されたのは1954年である1). まさにパンドラの箱として発見されたROSも, 現在までの54年の歳月を経て, 老化, 腫瘍, 糖尿病, 動脈硬化, 慢性関節リウマチなどの細胞機能制御因子として詳細な検討が行われてきた. 急性期管理医学領域のターゲットとする全身性炎症や虚血性病態においても, ROSで酸化された蛋白, 脂質, DNAが主要臓器機能に影響を与えることが注目されてきた. 傷害組織では, 浸潤する単球や好中球などの貪食細胞からROSが多量に放出されることに加えて, 組織を構成する様々な細胞が独自にROSを産生する. 正常生体内ではROSは微量の調節により細胞分化, 細胞増殖, 免疫反応, 炎症反応, 酸素センサーとして機能しているが, 近年特に病態時における調節機構としてNADPHオキシダーゼ(NOX)のROS産生機構の研究が進んできた. |
|---|
| Practice | 基礎医学・関連科学 |
|---|
| Keywords | 全身性炎症反応症候群, 活性酸素, NADPH, NOX |
|---|
| English |
|---|
| Title | Pathophysiology of Impaired Redox Signaling in Systemic Inflammatory Response Syndrome |
|---|
| Subtitle | |
|---|
| Authors | Naoyuki Matsuda |
|---|
| Authors(kana) | |
|---|
| Organization | Department of Primary Care and Emergency Medicine, Kyoto University Graduate School of Medicine |
|---|
| Journal | Circulation Control |
|---|
| Volume | 30 |
|---|
| Number | 2 |
|---|
| Page | 72-81 |
|---|
| Year/Month | 2009/12 |
|---|
| Article | Report |
|---|
| Publisher | Japan Society of Circulation Control |
|---|
| Abstract | The presence of free radicals in biological materials was discovered less than 50 years ago. An excessive and sustained increase in reactive oxygen species (ROS) production has been implicated in the pathogenesis of many diseases including systemic inflammatory response syndrome (SIRS). The NADPH oxidase enzymes (NOXs) are a particularly important source of ROS that are implicated in redox signaling. The NOXs are proteins that transfer electrons across biological membranes. NOX 1/2/4 and the organizer subunits(p47phox) can be upregulated in several types of cell of peripheral tissues by activation of transcriptional factors such as NF-κB and AP-1 in SIRS. Then, at produced high concentrations of ROS, many types of cell can strongly activate NF-κB and AP-1 to induce inflammatory burst and multiple organ failure (MOF). Thus, ROS is activated primarily in NOX-positive inflammatory alert cells to penetrate into NOX-negative non-alert cells and to enhance transcriptional activity of NF-κB and AP-1 and expression of NOXs in major organs and vasculatures. This article reviews the evidence for an involvement of NOXs and the co-factors in progressing MOF in SIRS. A better understanding of the roles of NOX family may define novel therapeutic targets for the prevention of severe SIRS. |
|---|
| Practice | Basic medicine |
|---|
| Keywords | NADPH, NOX |
|---|