Why the study?
Most pre-clinical myocardial infarction models disrupt pericardial integrity, causing the loss of the homeostatic cellular milieu.
Does maintaining an intact pericardium improve cardiac functional recovery in a rodent model of myocardial infarction?
Does maintaining an intact pericardium improve cardiac functional recovery in a rodent model of myocardial infarction?
A novel rodent model of myocardial infarction with an intact pericardium demonstrates improved cardiac functional recovery and enables the study of pericardial immune cells in post-MI remodeling.
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Intact pericardium may aid post-MI recovery in mice; hypothesis-generating for pericardial immune studies, no clinical translation yet.
This protocol has shown that the pericardium and its contents play an essential anti-fibrotic role in the ischemic rodent model (coronary ligation to induce myocardial injury). The majority of pre-clinical myocardial infarction models require the disruption of pericardial integrity with loss of the homeostatic cellular milieu. However, recently a methodology has been developed by us to induce myocardial infarction, which minimizes pericardial damage and retains the heart's resident immune cell population. An improved cardiac functional recovery in mice with an intact pericardial space following coronary ligation has been observed. This method provides an opportunity to study inflammatory responses in the pericardial space following myocardial infarction. Further development of the labeling techniques can be combined with this model to understand the fate and function of pericardial immune cells in regulating the inflammatory mechanisms that drive remodeling in the heart, including fibrosis.
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Hassanabad et al. (2021) studied this question.
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