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研究分野生物医学と臨床科学医学微生物学医療用感染剤 (プリオンを含む)
研究分野
生物医学と臨床科学
医学微生物学
医療用感染剤 (プリオンを含む)
Ncor1のNsun2媒介 m5Cメチル化は,ミトコンドリア機能障害を促進することによって,セプシス誘発の心筋病を悪化させる.

Ncor1のNsun2媒介 m5Cメチル化は,ミトコンドリア機能障害を促進することによって,セプシス誘発の心筋病を悪化させる.

Chan Chen ¹, Qing Liu ¹, Junmei Xu ¹, Mengyuan Zi ¹, Xinglan Chen ¹, Feng Xiao ¹

Chan Chen ¹, Qing Liu ¹, Junmei Xu ¹

¹Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China.

⁰Department of Anesthesiology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China.

Free Radical Biology & Medicine +

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2026年1月1日

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2026年1月1日

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まとめ

No abstract available on PubMed

キーワード:

心筋細胞アポトーシスミトコンドリア分裂 Ncor1 について Nsun2 についてセプシス誘発性心筋病 (SIC) m5CRNAメチル化について

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Contact us これらのビデオが関連しない場合は

<em>In Vivo</em> Nanovector Delivery of a Heart-specific MicroRNA-sponge

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Published on: June 15, 2018

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関連する概念動画

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

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