相关实验视频
Updated: Jun 15, 2025

05:14
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
4.5K
下调miR-432-5p通过激活RTN3信号通路来加剧阿德里亚米辛诱导的心脏毒性
Wei Geng1, Shaohua Yan1, Dasen Sang1
1Department of Cardiology, Baoding No.1 Central Hospital, Baoding, Hebei Province, China.
Aging
|August 23, 2024
概括
阿德里亚米 (ADR) 化学疗法通过减少miR-432-5p和损害线粒体功能而导致心脏毒性. 恢复miR-432-5p通过降低ER压力和RTN3通路的调节来保护心脏.
科学领域:
- 心脏病学 心脏病学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 阿德里亚米 (ADR) 是一种重要的化疗剂,已知具有心脏毒性.
- 心肌细胞表达miR-432-5p,它具有保护性质.
- 由ADR引起的心脏毒性包括线粒体ATP代谢受损和内质网膜应激 (ERs).
研究的目的:
- 调查miR-432-5p对ADR诱导的心脏毒性的保护作用.
- 阐明miR-432-5p对心肌细胞中的线粒体ATP代谢和ER压力的影响.
主要方法:
- 使用初级心肌细胞和小鼠模型来评估ADR影响和miR-432-5p水平.
- miR-432-5p在体外和体内进行了介绍,以评估其对ATP合成,自和ER压力的影响.
- 生物信息学分析确定了miR-432-5p的目标.
主要成果:
- 治疗ADR减少了心肌细胞中的miR-432-5p表达.
- ADR降低了线粒体ATP的产生,并激活了ER压力,通过增加LC3B,Beclin 1和裂开的caspase 3来表明.
- 外源性miR-432-5p补充剂通过降低ER相关RTN3信号通路的调节来减轻ADR诱导的心脏毒性.
结论:
- 通过减少miR-432-5p表达和激活ER RTN3通路,ADR诱导心脏毒性.
- 这种激活导致LC3B,Beclin 1,切割caspase 3,CHOP和RTN3.3的表达增加.
- miR-432-5p在保护心肌细胞免受ADR引起的损伤方面发挥着至关重要的作用.
相关概念视频
mTOR Signaling and Cancer Progression
3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.8K
PI3K/mTOR/AKT Signaling Pathway
3.4K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.4K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
405
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
405
MicroRNAs
21.2K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
21.2K
MAPK Signaling Cascades
5.3K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.3K

