Suppr超能文献

一种时空心肌细胞靶向载体系统,可有效递送电疗有效载荷,以消退心脏肥大的旁观者效应。

A spatio-temporal cardiomyocyte targeted vector system for efficient delivery of therapeutic payloads to regress cardiac hypertrophy abating bystander effect.

机构信息

Department of Zoology, University of Calcutta, 35, B.C. Road, Kolkata 700019, India.

Centre for Chemical Biology, Indian Institute of Chemical Technology, Uppal Road, Hyderabad 500007, India.

出版信息

J Control Release. 2015 Feb 28;200:167-78. doi: 10.1016/j.jconrel.2015.01.008. Epub 2015 Jan 7.

Abstract

Diverse array of therapeutic regimens, drugs or siRNA, are commonly used to regress cardiac hypertrophy, although, bystander effect and lower retention of bioactive molecules significantly reduce their functional clinical efficacy. Carvedilol, a widely used and effective anti-hypertrophic drug, simultaneously blocks β-adrenergic receptors non-specifically in various organs. Likewise, non-specific genome-wide downregulation of p53 expression by specific siRNA efficiently abrogates cardiac hypertrophy but results in extensive tumorigenesis affecting bystander organs. Therefore, delivery of such therapeutics had been a challenge in treating cardiovascular dysfunction. Cardiac tissue engineering was successfully accomplished in this study, by encapsulating such bioactive molecules with a stearic acid modified Carboxymethyl chitosan (CMC) nanopolymer conjugated to a homing peptide for delivery to hypertrophied cardiomyocytes in vivo. The peptide precisely targeted cardiomyocytes while CMC served as the vector mediator to pathological myocardium. Controlled delivery of active therapeutic payloads within cardiomyocytes resulted in effective regression of cardiac hypertrophy. Thus, this novel nano-construct as a spatio-temporal vector would be a potential tool for developing effective therapeutic strategies within cardiac micro-environment via targeted knockdown of causal genes.

摘要

多种治疗方案、药物或 siRNA 常用于逆转心肌肥厚,但旁观者效应和生物活性分子的保留率较低,显著降低了它们的临床疗效。卡维地洛是一种广泛应用且有效的抗肥厚药物,它在多种器官中同时非特异性地阻断β-肾上腺素能受体。同样,通过特异性 siRNA 非特异性地下调全基因组 p53 表达可有效抑制心肌肥厚,但会导致广泛的肿瘤形成,影响旁观者器官。因此,这些治疗药物的输送一直是治疗心血管功能障碍的一个挑战。本研究通过将这种生物活性分子与一种经过硬脂酸修饰的羧甲基壳聚糖(CMC)纳米聚合物偶联,该聚合物偶联有一个归巢肽,用于在体内递送至肥厚的心肌细胞,成功地实现了心脏组织工程。该肽能精确靶向心肌细胞,而 CMC 则作为载体介导物作用于病理性心肌。在心肌细胞内实现活性治疗有效载荷的控制释放,可有效逆转心肌肥厚。因此,这种新型纳米构建体作为时空载体,可能是通过靶向敲除因果基因,在心脏微环境中开发有效治疗策略的潜在工具。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验