This review summarizes the cellular effectors and molecular signals regulating inflammatory and reparative responses after myocardial infarction, highlighting recent data in cardiovascular immunotherapy.
Myocardial infarction
Despite recent scientific and technological advances, myocardial infarction (MI) still represents a major global health problem, leading to high morbidity and mortality worldwide. During the post-MI wound healing process, dysregulated immune inflammatory pathways and failure to resolve inflammation are associated with maladaptive left ventricular remodeling, progressive heart failure, and eventually poor outcomes. Given the roles of immune cells in the host response against tissue injury, understanding the involved cellular subsets, sources, and functions is essential for discovering novel therapeutic strategies that preserve the protective immune system and promote optimal healing. This review discusses the cellular effectors and molecular signals across multi-organ systems, which regulate the inflammatory and reparative responses after MI. Additionally, we summarize the recent clinical and preclinical data that propel conceptual revolutions in cardiovascular immunotherapy.
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Atsushi Anzai
Keio University
Seien Ko
Keio University
Keiichi Fukuda
Heart Failure & Transplant
International Journal of Molecular Sciences
Keio University
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Anzai et al. (Fri,) conducted a review in Myocardial infarction. This review summarizes the cellular effectors and molecular signals regulating inflammatory and reparative responses after myocardial infarction, highlighting recent data in cardiovascular immunotherapy.
synapsesocial.com/papers/6a18e118c9d74cf65281fc64 — DOI: https://doi.org/10.3390/ijms23095214