About this Research Topic
Myocardial infarction (MI) represents a critical global health challenge, imposing a substantial economic burden and standing as a leading contributor to cardiovascular morbidity and mortality. This condition, characterized by the irreversible consequences of coronary artery ischemia, predisposes patients to heart failure, significantly affecting their quality of life and long-term prognosis. The activation of the inflammatory immune response following MI plays a pivotal role in the repair processes of myocardial tissue. However, an excessive inflammatory reaction exacerbates infarct size and intensifies adverse cardiac remodeling. In recent years, the cardiovascular research community has achieved significant advancements in elucidating the complex mechanisms and molecular underpinnings of inflammation in the context of MI. These efforts have also led to a deeper understanding of the long-term clinical trajectory and the emergence of novel therapeutic strategies aimed at mitigating inflammation-related damage.
Despite these advancements, substantial global uncertainties and disparities continue regarding the specific mechanisms through which inflammation influences MI pathophysiology, underscoring the need for ongoing research.. This research topic aims to elucidate the intricate mechanisms of inflammation in MI and explore innovative immunomodulatory strategies that can directly enhance cardiac repair post-infarction. A particular focus will be the examination of the roles played by monocytes, macrophages, natural killer cells, T cells, and other engineered immune cells in the context of cardiac remodeling following MI.
The objective of this research topic is to serve as a comprehensive platform for advancing our understanding of the inflammatory pathways implicated in MI. From a clinical translation perspective, the issue will delve into cutting-edge immunomodulatory strategies designed to mitigate myocardial remodeling by precisely targeting and modulating immune cell activity to resolve inflammation. Additionally, it will explore the potential of rationally designed nanoparticles and biomaterials to induce immune modulation, thereby inhibiting the activation of pro-inflammatory signaling pathways. By fostering a deeper understanding of these mechanisms, this special issue seeks to contribute to the development of novel therapeutic approaches for improving patient outcomes in the aftermath of myocardial infarction.
We welcome submissions on the following topics, but are not limited to:
- The intricate biological mechanisms underlying the development of inflammation during myocardial infarction and its complex interplay with post-infarction myocardial remodeling.
- The identification and characterization of inflammation-related biomarkers, focusing on their diagnostic value in the onset, progression, and prognosis of myocardial infarction.
- The role and mechanistic pathways of immune inflammation-related cells in the pathophysiology of myocardial infarction, emphasizing their contribution to disease progression.
- Innovations in techniques and methodologies for the manipulation and modification of immune cells, aimed at therapeutic intervention in myocardial remodeling following infarction.
Despite these advancements, substantial global uncertainties and disparities continue regarding the specific mechanisms through which inflammation influences MI pathophysiology, underscoring the need for ongoing research.. This research topic aims to elucidate the intricate mechanisms of inflammation in MI and explore innovative immunomodulatory strategies that can directly enhance cardiac repair post-infarction. A particular focus will be the examination of the roles played by monocytes, macrophages, natural killer cells, T cells, and other engineered immune cells in the context of cardiac remodeling following MI.
The objective of this research topic is to serve as a comprehensive platform for advancing our understanding of the inflammatory pathways implicated in MI. From a clinical translation perspective, the issue will delve into cutting-edge immunomodulatory strategies designed to mitigate myocardial remodeling by precisely targeting and modulating immune cell activity to resolve inflammation. Additionally, it will explore the potential of rationally designed nanoparticles and biomaterials to induce immune modulation, thereby inhibiting the activation of pro-inflammatory signaling pathways. By fostering a deeper understanding of these mechanisms, this special issue seeks to contribute to the development of novel therapeutic approaches for improving patient outcomes in the aftermath of myocardial infarction.
We welcome submissions on the following topics, but are not limited to:
- The intricate biological mechanisms underlying the development of inflammation during myocardial infarction and its complex interplay with post-infarction myocardial remodeling.
- The identification and characterization of inflammation-related biomarkers, focusing on their diagnostic value in the onset, progression, and prognosis of myocardial infarction.
- The role and mechanistic pathways of immune inflammation-related cells in the pathophysiology of myocardial infarction, emphasizing their contribution to disease progression.
- Innovations in techniques and methodologies for the manipulation and modification of immune cells, aimed at therapeutic intervention in myocardial remodeling following infarction.
Keywords: inflammation, myocardial infarction, coronary artery disease, heart failure, cardiovascular disease
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
