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Published online: 2 September 2009 | doi:10.1038/nchina.2009.174

Cardiology: Heart therapy

Felix Cheung

Introduction

© (2009) istockphoto.com/Max Delson Martins Santos

Integrin-linked kinase (ILK) is a protein kinase that is highly expressed in the heart. Recent studies suggest that ILK may have therapeutic potential for the treatment of myocardial infarction (the death of cardiac muscle cells). Biao Xu at Nanjing University, Albert Ferro at King's College London and co-workers¹ have now shown that ILK gene therapy can improve the left ventricular and cardiac function after myocardial infarction.

The researchers injected ILK-expressing or null vectors into rats that had undergone left anterior descending artery ligation — a technique commonly used to induce myocardial infarction for research purposes. Four weeks after the injection, they found that 'ILK-treated' rats showed improved cardiac function in comparison to 'null' rats.

The left ventricles of ILK-treated rats also showed signs of improvement, including reduced infarct scar size, preserved diameter and increased wall thickness. In addition, the cardiac muscle cells showed increased angiogenesis, reduced apoptosis and increased proliferation.

Nine weeks after the injection, the researchers could find little difference in the cardiac function between ILK-treated and normal rats. ILK gene therapy may therefore represent a new approach to the treatment of myocardial infarction and subsequent heart failure.

The authors of this work are from:
Department of Cardiology, Drum Tower Hospital, Medical School, Nanjing University, Nanjing, China; State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China; Department of Clinical Pharmacology, Cardiovascular Division, School of Medicine, King's College London, London, UK.

Reference

1. Ding, L. et al. Increased expression of integrin-linked kinase attenuates left ventricular remodeling and improves cardiac function after myocardial infarction. Circulation doi:10.1161/CIRCULATIONAHA.109.870725 (2009). | Article