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Endocannabinoids and Cardiovascular Diseases

We investigate innate immune responses and endocannabinoid signaling in cardiac repair and vascular disease.

We investigate innate immune responses and endocannabinoid signaling in cardiac repair and vascular disease.

About our research

Lipid signaling in cardiovascular disease

Lipid mediators derived from the essential fatty acid arachidonic acid play pivotal roles in acute inflammatory responses, resolution of inflammation as well as chronic inflammation such as atherosclerosis. Endocannabinoids are one group of arachidonic acid-derived lipid mediators, which bind to cannabinoid receptors CB1 and CB2. A few years ago, the orphan receptor GPR55 has been proposed as a novel cannabinoid receptor, although this designation remains somewhat controversial. In fact, lysophosphatidylinositols (LPIs) are more potent endogenous GPR55 ligands than endocannabinoids. We are generally studying how lipid mediators and their specific receptors affect acute and chronic cardiovascular disease manifestations.


Chronic inflammation in atherosclerosis and related metabolic disorders

It is known that tissue and circulating levels of endocannabinoids and fatty acid amide analogues are dysregulated in atherosclerosis and its related cardiovascular risk factors, obesity, dyslipidemia, diabetes and endothelial dysfunction. However, the pathophysiological effect of this dysregulated tone in cardiovascular disease is not well understood. Our group aims to clarify the precise pathophysiological relevance of these receptors and ligands in cardiovascular disease. This might open new avenues for biomarker research and therapeutic interventions.


Myocardial infarction and repair

Myocardial infarction induces an inflammatory response, which is required for the induction of cardiac repair processes. Various cell types, including neutrophils and macrophages, are involved at different stages of infarct healing, ultimately leading to scar formation and adaptive remodeling to preserve cardiac function. The inflammatory response after MI needs to be well-balanced in order to limit infarct expansion and progressive loss of cardiac function. In this regard, our research aims at better understanding the signaling pathways and local (lipid) regulators in the cardiac microenvironment promoting resolution of inflammation and favorable healing responses. Recently, we identified the pericardial adipose tissue as a crucial regulator of post-myocardial infarction immune responses. Our findings suggests that the pericardial adipose tissue is a preferential site for innate-adaptive immune cell cross talk and lymphocyte activation, with important consequences for cardiac healing.


Adverse cardiac remodeling and heart failure

Heart failure is a state of chronic inflammation, characterized by heightened levels of circulating and myocardial proinflammatory cytokines that promote pathological left ventricular remodeling. Chronic heart failure is generally associated with poor prognosis and high mortality rate, depending on the severity of systolic dysfunction. Heart failure can have multiple causes, such as ischemic injury or cardiac overload, inflammatory, biochemical or neurohormonal changes acting on the myocardium. We aim to clarify the role of the pericardial adipose tissue lymphoid clusters and underlying cues for immune cell activation in this pathophysiological condition.


Models and techniques used in the lab

Mouse models of atherosclerosis, myocardial infarction, angiotensin 2-induced cardiac hypertrophy, TAC-induced hypertrophy, mini-pump implantation, echocardiographic assessment of cardiac function parameters, intraventricular pressure-volume catheter

Contact Us

Prof. Dr. Sabine Steffens

Group Leader Cardiovascular Disease Comorbidities