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Unraveling the thread of uncontrolled immune response in COVID-19 and STEMI: an emerging need for knowledge sharing
Cesar Rios-Navarro1, Elena de Dios2,3, Maria J Forteza4
1INCLIVA Health Research Institute, University of Valencia, Valencia, Spain.
Insights
Severe immune deregulation in ST-elevation myocardial infarction and coronavirus disease 2019 mirrors inflammatory cell changes. Understanding these immune responses may reveal new therapies for critical illnesses.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- The coronavirus disease 2019 (COVID-19) pandemic highlights the need for knowledge sharing regarding severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
- Myocardial infarction remains a leading cause of death, with immune system deregulation potentially exacerbating critical illness and organ failure.
- Shared immune responses, including neutrophilia, monocytosis, and lymphopenia, are observed in both severe COVID-19 and ST-elevation myocardial infarction.
Purpose of the Study:
- To explore the cellular and molecular mechanisms of immune response activation and downregulation in myocardial infarction and COVID-19.
- To enhance understanding of the pathophysiology linking these critical conditions.
- To identify potential innovative therapeutic strategies for reducing mortality in both infectious and non-infectious diseases.
Main Methods:
- Review of existing literature on immune cell dynamics in ST-elevation myocardial infarction and COVID-19.
- Comparative analysis of inflammatory profiles in severe cases of both conditions.
- Examination of molecular pathways governing innate and adaptive immunity.
Main Results:
- A proinflammatory imbalance, favoring innate over adaptive immunity, is associated with adverse outcomes in both conditions.
- The immune cell profiles in severe ST-elevation myocardial infarction closely resemble those reported in severe COVID-19.
- Deregulation of the immune system contributes to exaggerated inflammatory responses and multi-organ failure.
Conclusions:
- Shared immune mechanisms in myocardial infarction and COVID-19 offer therapeutic targets.
- Further research into these immune pathways could lead to novel treatments for critical illnesses.
- Knowledge sharing is crucial for developing therapies to reduce mortality across diverse medical scenarios.
Abstract:
The outbreak of severe acute respiratory syndrome coronavirus 2 that first emerged in Wuhan in December 2019 has resulted in the devastating pandemic of coronavirus disease 2019, creating an emerging need for knowledge sharing. Meanwhile, myocardial infarction is and will probably remain the foremost cause of death in the Western world throughout the coming decades. Severe deregulation of the immune system can unnecessarily expand the inflammatory response and participate in target and multiple organ failure, in infection but also in critical illness. Indeed, the course and fate of inflammatory cells observed in severe ST-elevation myocardial infarction (neutrophilia, monocytosis, and lymphopenia) almost perfectly mirror those recently reported in severe coronavirus disease 2019. A pleiotropic proinflammatory imbalance hampers adaptive immunity in favor of uncontrolled innate immunity and is associated with poorer structural and clinical outcomes. The goal of the present review is to gain greater insight into the cellular and molecular mechanisms underlying this canonical activation and downregulation of the two arms of the immune response in both entities, to better understand their pathophysiology and to open the door to innovative therapeutic options. Knowledge sharing can pave the way for therapies with the potential to significantly reduce mortality in both infectious and noninfectious scenarios.
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