Recovery from myocardial infarction is associated with a series of alterations in heart structure and function, collectively known as cardiac remodelling, which play a major role in the subsequent development of heart failure.

Early remodelling involves infarct scar formation in the ischaemic zone whereas subsequent ventricular remodelling affects mainly the viable non-infarcted myocardium with especially profound alterations in the extracellular matrix.

There is growing evidence for a role of oxidative stress and redox signalling in the processes underlying cardiac remodelling.

Reactive oxygen species are a group of highly reactive molecules which have the potential to modulate several biological processes as well as cause tissue damage and dysfunction. Their effects can be beneficial or deleterious, depending on the concentrations produced, the site of production, and the overall redox status of the cell.

Reactive oxygen species can be generated by all cardiovascular cell types.

Under pathophysiological conditions, major enzymatic sources appear to be mitochondria, xanthine oxidase and the non-phagocytic NADPH oxidases.

In this review, we outline the mechanisms underlying the progression of early and late cardiac remodelling with particular focus on the role of oxidative stress and the potential sources of reactive oxygen species which may be involved.