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微小RNA 是一组高度保守的长度约22 个核苷酸非编码RNA，通过靶定相应的互补序列导致信使RNA的沉默，下调或者抑制翻译以调节基因和蛋白的表达。心力衰竭进程中存在慢性炎症激活和microRNA的异常表达，其中TLR4 通路和NF-资B 通路被广泛研究和认同，炎症因子如IL-1、IL-6、TNF-琢参与心力衰竭的炎症激活过程，并且可以通过多种通路导致心肌细胞肥大，纤维化及凋亡，炎症因子激活、炎症通路中间因子及疾病进展形成复杂的病理网络，最终导致心肌功能紊乱和减退；microRNA 可通过部分结合mRNA靶定部分在转录水平上抑制蛋白合成，参与心力衰竭炎症通路的整个过程，这一调节机制在心肌肥大、心力衰竭等多种心脏疾病中的作用逐渐被阐明。本文旨在总结微小RNAs在心力衰竭炎症机制中作用的研究进展，寻找微小RNA与心力衰竭中炎症激活过程的联系。

英文摘要:

It is necessary for the conservation and genomic stability and integrity of chromatin to prevent from various factors causing continuous damage and keep cell maintain normal growth, division and reproduction in vitro and vivo. ATP- Dependent Chromatin-Remodeling that is one of the most important way of DNA damage repair response mainly exposure chromatin condensation by the energy of ATP hydrolysis and coordinate effect of the damage repair protein and the sites of DNA damage by histone covalent modifications or ATP- Dependent Chromatin-Remodeling Complexes which open the door of DNA damage repair response.It is recently reported that CHD4 can participate in the regulation of DNA damage repair with functions of chromatin remodeling. It is very important that the second PHD finger (PHD2) of CHD4 recognizes the N-terminus of histone H3 and that this interaction is facilitated by acetylation ormethylation of Lys9(H3K9ac andH3K9me respectively) but is inhibited by methylation of Lys4(H3K4me) or acetylation of Ala1 (H3A1ac) to provide protection for chromatin remodeling. Mi-2β/ CHD4 is Colocalization with γ-H2AX foci in the DNA damage response. Silence Mi - 2 beta/CHD4 genes, cells increase spontaneous DNA damage and radiation sensitivity. Show CHD4 in chromatin remodeling plays an important role.Silence Mi-2β/CHD4 regulates cell sensitivity to spontaneous DNA damage and radiosensitivity. CHD4 has an important role in chromatin remodeling.

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