Reversing Cardiac Hypertrophy at the Source Using a Cardiac Targeting Peptide Linked to miRNA106a: Targeting Genes That Cause Cardiac Hypertrophy.
Reversing Cardiac Hypertrophy at the Source Using a Cardiac Targeting Peptide Linked to miRNA106a: Targeting Genes That Cause Cardiac Hypertrophy.
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DOI：
10.3390/ph15070871
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发表时间：
2022-07-15
期刊：
影响因子：
4.6
通讯作者：
Zahid, Maliha
中科院分区：
文献类型：
--
作者：
Gallicano, G. Ian;Fu, Jiayu;Mahapatra, Samiksha;Sharma, Michael V. R.;Dillon, Conor;Deng, Claire;Zahid, Maliha
心力衰竭（HF）的病因和治疗方法已经研究了一个多世纪，最终的数据导致了许多药物和手术治疗。不幸的是，到目前为止，即使采用最先进的治疗方法，心衰仍然是一种进行性疾病，没有直接针对心肌细胞的治疗方法。过去两到三年的技术进步为治疗许多以前极其难以解决的疾病带来了新的范例。这些新范式之一是从药理学药物转向反义技术（例如，microrna），以靶向导致疾病发病的病理过程的分子基础。虽然这种模式的转变可能在十多年前就已经提出，但直到最近几年才变得可行。在这里，我们发现miRNA106a靶向基因，当失调时，已被证明会导致肥大和最终HF。miRNA106a的加入抑制错误表达的HF基因并逆转肥厚。最重要的是，使用与miRNA106a可逆关联的心脏靶向肽，我们发现递送对心肌细胞具有特异性。
Causes and treatments for heart failure (HF) have been investigated for over a century culminating in data that have led to numerous pharmacological and surgical therapies. Unfortunately, to date, even with the most current treatments, HF remains a progressive disease with no therapies targeting the cardiomyocytes directly. Technological advances within the past two to three years have brought about new paradigms for treating many diseases that previously had been extremely difficult to resolve. One of these new paradigms has been a shift from pharmacological agents to antisense technology (e.g., microRNAs) to target the molecular underpinnings of pathological processes leading to disease onset. Although this paradigm shift may have been postulated over a decade ago, only within the past few years has it become feasible. Here, we show that miRNA106a targets genes that, when misregulated, have been shown to cause hypertrophy and eventual HF. The addition of miRNA106a suppresses misexpressed HF genes and reverses hypertrophy. Most importantly, using a cardiac targeting peptide reversibly linked to miRNA106a, we show delivery is specific to cardiomyocytes.
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