相关实验视频
Updated: Sep 10, 2025

09:53
In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
7.6K
肺高血压中的miRNAs:机制见解和治疗潜力
Jindong Fang1,2,3, Hongyang Chen1,2,3, Zhuangzhuang Jia1,2,3
1School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.
Biomedicines
|August 28, 2025
概括
微RNAs (miRNAs) 显示出调节肺高血压 (PH) 发病的潜力,作为生物标志物和治疗剂. 需要进一步的研究将这些发现转化为PH的临床应用.
科学领域:
- 生物医学研究
- 分子生物学
- 心血管研究
背景情况:
- 肺高血压是一种严重的血管疾病.
- 主要的致病机制包括血管重塑,代谢重编程,炎症和纤维化.
- 微RNA (miRNA) 是调节基因表达的小型非编码RNA.
研究的目的:
- 审查miRNAs在PH病变中的作用.
- 探索miRNAs作为PH的生物标志物的潜力.
- 讨论miRNAs作为PH的治疗剂.
主要方法:
- 关于miRNAs和PH的文献综述
- 在PH中分析miRNA调节机制.
- 综合目前的实验结果.
主要成果:
- 在PH的发病过程中涉及miRNAs.
- miRNAs 显示出作为诊断生物标志物的潜力.
- miRNAs为新的治疗策略提供了前景.
结论:
- 在PH中,miRNAs起着重要的调节作用.
- 将miRNA研究转化为临床实践需要进一步的研究.
- 在PH诊断和治疗中miRNAs的未来应用是有希望的.
相关概念视频
Pulmonary Hypertension: Classification and Pathogenesis
284
Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
There are various classifications for PH, each relating to different underlying causes and also...
284
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
253
Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
253
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
223
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
223
MicroRNAs
3.1K
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 the pre-miRNA...
3.1K
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
251
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
251

