인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Reactive oxygen species (ROS) can induce oxidative injury and are generally regarded as toxic byproducts, although they are increasingly recognized for their signaling functions. Increased ROS often accompanies liver regeneration (LR) after liver injuries, however, their role in LR and the underlying mechanism remains unclear. Here, by employing a mouse LR model of partial hepatectomy (PHx), we found that PHx induced rapid increases of mitochondrial hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and intracellular H<sub>2</sub>O<sub>2</sub> at an early stage, using a mitochondria-specific probe. Scavenging mitochondrial H<sub>2</sub>O<sub>2</sub> in mice with liver-specific overexpression of mitochondria-targeted catalase (mCAT) decreased intracellular H<sub>2</sub>O<sub>2</sub> and compromised LR, while NADPH oxidases (NOXs) inhibition did not affect intracellular H<sub>2</sub>O<sub>2</sub> or LR, indicating that mitochondria-derived H<sub>2</sub>O<sub>2</sub> played an essential role in LR after PHx. Furthermore, pharmacological activation of FoxO3a impaired the H<sub>2</sub>O<sub>2</sub>-triggered LR, while liver-specific knockdown of FoxO3a by CRISPR-Cas9 technology almost abolished the inhibition of LR by overexpression of mCAT, demonstrating that FoxO3a signaling pathway mediated mitochondria-derived H<sub>2</sub>O<sub>2</sub> triggered LR after PHx. Our findings uncover the beneficial roles of mitochondrial H<sub>2</sub>O<sub>2</sub> and the redox-regulated underlying mechanisms during LR, which shed light on potential therapeutic interventions for LR-related liver injury. Importantly, these findings also indicate that improper antioxidative intervention might impair LR and delay the recovery of LR-related diseases in clinics.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.