Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we will assume that you are happy to receive all cookies and you will not see this message again. Click 'Find out more' for information on how to change your cookie settings.

Despite decades of research, regeneration of the infarcted human heart remains an unmet ambition. A significant obstacle facing experimental regenerative therapies is the hostile immune response which arises following a myocardial infarction (MI). Upon cardiac damage, sterile inflammation commences via the release of pro-inflammatory meditators, leading to the migration of neutrophils, eosinophils and monocytes, as well as the activation of local vascular cells and fibroblasts. This response is amplified by components of the adaptive immune system. Moreover, the physical trauma of the infarction and immune-mediated tissue injury provides a supply of autoantigens, perpetuating a cycle of autoreactivity, which further contributes to adverse remodelling. A gradual shift towards an immune-resolving environment follows, culminating in the formation of a collagenous scar, which compromises cardiac function, ultimately driving the development of heart failure. Comparing the human heart with those of animal models that are capable of cardiac regeneration reveals key differences in the innate and adaptive immune responses to MI. By modulating key immune components to better resemble those of regenerative species, a cardiac environment may be established which would, either independently or via the synergistic application of emerging regenerative therapies, improve functional recovery post-MI.

Original publication

DOI

10.1038/s41536-021-00118-2

Type

Journal article

Journal

NPJ Regen Med

Publication Date

15/02/2021

Volume

6