Decoding Long Noncoding RNAs in Myocardial Infarction: A Step Closer to a "Magic Bullet"?

Ischaemic heart disease (IHD) remains the greatest cause of global mortality. 1 Vaduganathan M. Mensah G.A. Turco J.V. Fuster V. Roth G.A. The Global Burden of Cardiovascular Diseases and Risk: A Compass for Future Health. J Am Coll Cardiol. 2022; 80: 2361-2371 Crossref PubMed Scopus (205) Google Scholar The success of early primary percutaneous coronary intervention (PPCI) has resulted in an unprecedented number of patients surviving acute myocardial infarction (MI), but they are vulnerable to progressing into heart failure due to a loss of functional myocardium. During MI, damaged tissue initiates an inflammatory cascade, instigated by pro-inflammatory molecules, such as damage-associated molecular patterns (DAMPs) which are recognised by pattern recognition receptors, e.g., the extracellular toll-like receptors 2 (TLR2) and 4 (TLR4). The early inflammatory response, characterised by activation of resident and infiltration of circulating immune cells, is a double-edged sword. 2 Cheng B. Chen H.C. Chou I.W. Tang T.W. Hsieh P.C. Harnessing the early post-injury inflammatory responses for cardiac regeneration. J Biomed Sci. 2017; 24: 7 Crossref PubMed Scopus (36) Google Scholar ,3 Epelman S. Lavine K.J. Beaudin A.E. et al. Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. Immunity. 2014; 40: 91-104 Abstract Full Text Full Text PDF PubMed Scopus (1005) Google Scholar While it prevents rupture, removes cellular debris and promotes wound healing, excessive, unresolved inflammation precipitates adverse cardiac remodelling and functional impairment. 4 Matter M.A. Paneni F. Libby P. et al. Inflammation in acute myocardial infarction: the good, the bad and the ugly. Eur Heart J. 2023; PubMed Google Scholar By better understanding the molecular and cellular players that fine-tune the inflammatory response post-MI, there is a therapeutic opportunity to prevent the heart’s functional decline. LncRNA CCRR Attenuates Post-Myocardial Infarction Inflammatory Response by Inhibiting the TLR Signaling PathwayCanadian Journal of CardiologyPreviewTimely and proper suppression of inflammation can effectively reduce myocardial injury and promote post-myocardial infarction (post-MI) wound healing process. We have previously found that cardiac conduction regulatory RNA (CCRR), a long noncoding RNA (lncRNA) transcribed by the gene located on chromosome 9 with abundant expression in the heart, elicits anti-arrhythmic effects in heart failure, and this is a continuing study on the role of CCRR in MI. Full-Text PDF