Dr. Abdel-Latif is a clinician-scientist in the division of Cardiology, with a productive track record in basic and translational studies focused on the molecular and cellular mechanisms of pathological cardiac remodeling. He is trained as an interventional cardiologist and immunologist. He has a long-standing track record of multi-investigator collaborations that resulted in seminal observations in the field. His lab explores the molecular and cellular response to myocardial stress and its role in cardiac remodeling. To this goal, the lab integrates clinical, biochemical, cellular, and pharmacological methods to examine the role of bone marrow-derived innate immune cells in cardiac disease. As an interventional cardiologist and physician-scientist, he routinely provides care for patients affected by cardiovascular disease and is well-versed in the challenges and limitations of current treatments in reducing the initial damage caused by cardiac injury and the clinical implications of heart failure. He also has considerable experience in translational research spanning basic research, human translational projects, and multi-center clinical studies.
Dr. Abdel-Latif has been actively mentoring students, postdoctoral fellows, and clinical fellows. Over the past 11 years, he has served on 10 Ph.D. committees. He has mentored 5 postdoc fellows (3 of which won prestigious awards such as the T32 fellowship and 3 are in academia). Collectively, he has mentored an additional 11 undergraduate students in his laboratory. Many of these trainees have published or won prestigious research awards.

Heart failure affects around 23 million people worldwide each year, however there are currently no curative treatments. The most common cause of heart failure is heart attack during which, an adult heart can lose up to one billion cardiomyocytes. Unlike many other organs in the body, the adult heart cannot regenerate itself and lost cardiomyocytes cannot be replaced. This leads to weakness of the heart muscle, scar formation and eventually patient death.

Following a heart attack, the body's immune system initiates a reparative process to restore the damaged heart muscle. However, if this response persists for an extended period, it can exacerbate heart damage. The precise mechanisms governing the activation and regulation of this immune response remain incompletely elucidated. Intriguingly, there exists a close association between the immune response and the regenerative capacity of the heart. In contrast to higher organisms, more primitive organisms and mammalian neonates possess a remarkable ability to regenerate their heart tissue, which has been attributed to their comparatively rudimentary (immature) immune response to tissue injury. In our laboratory, we employ innovative comparative biology models to further investigate the intricate interactions between immune cells, mature cardiac cells, and stem cells, with the ultimate goal of enhancing cardiac functional recovery following a heart attack.

Our laboratory is dedicated to elucidating the molecular mechanisms underlying heart failure and investigating the intricate involvement of the immune system in this process. To accomplish this, we employ a combination of animal models and clinical studies, which serve as the foundation for our experimental investigations. In particular, our research highlights the critical role played by key components of the immune system, such as neutrophils and macrophages, in both cardiac inflammation and the subsequent recovery phase.

Macrophages, in particular, are indispensable for promoting tissue healing following injury, extending their influence to almost every organ within the body. However, in the context of a heart attack, prolonged pro-inflammatory activation of macrophages can instead contribute to cardiac damage. Therefore, a highly promising strategy to mitigate the initial extent of cardiac injury (preservation) post-heart attack involves modulating the activation state of macrophages, steering them towards an anti-inflammatory phenotype referred to as alternative polarization.

In our laboratory, we pursue diverse approaches aimed at enhancing alternative macrophage polarization. These methodologies encompass not only cell therapy interventions but also the exploration of various novel and repurposed pharmaceutical agents. Through these comprehensive investigations, we aim to expand our understanding of the immune response in cardiac pathology and identify potential therapeutic avenues to improve patient outcomes in the context of heart failure.