New evidence of cross-disease communication between heart and liver

Abstract

Section snippets

Background and context

Much is known about the cardiovascular implications of metabolic dysfunction-associated steatohepatitis (MASH). Cardiovascular disease (CVD) represents the leading cause of mortality in patients with MASH and despite overlapping risk factors for both conditions, the presence of hepatic steatosis and inflammation are generally regarded as independent risk factors for ischaemic heart disease (IHD).^1,2 This is likely to occur through a combination of liver-derived systemic inflammation,

Objectives, methods and findings

This work predominantly involved subjecting rodents with and without MASH to acute MI (via ligating the left anterior descending coronary artery) or sham surgery. Authors then characterised the liver phenotype, hepatic cell infiltrate, and systemic immune response to intervention, before using a range of treatment conditions to offer mechanistic insights into the cellular and soluble mediators of post-MI liver damage. Firstly, MI was found to exacerbate liver injury in three different models of

Scientific importance and translational relevance

There is still some way to go before the concept of accelerated liver damage after MI is considered a major shift in our understanding of human MASH. The mechanistic components of the current work are performed entirely in preclinical models and further investigation is now required as part of clinical studies, not least because both lipid metabolism and cardiovascular structure differ between rodents and humans.^11,12 In addition, a single assessment of liver pathology was made at 14 days after

Financial support

T.M. is supported by a National Institute for Health Research (NIHR) Academic Clinical Lectureship. The views expressed are those of the author and not necessarily those of the National Health Service (NHS), the NIHR or the Department of Health.

Conflict of interest

T.M. has no conflicts of interest to declare.Please refer to the accompanying ICMJE disclosure forms for further details.

Acknowledgements

T.M. would like to thank Dr Paul N Brennan (University of Dundee, UK) for an informal check of the initial article draft.