Molecular Cardiology Research Institute (MCRI)

The Molecular Cardiology Research Institute (MCRI) at Tufts Medical Center is dedicated to investigating the molecular mechanisms of common cardiovascular diseases and translating those discoveries into new clinical strategies for diagnosis and therapy to prevent and treat various forms of heart disease including heart attack, high blood pressure and heart failure.

MCRI tripartite mission

The MCRI is comprised of 12 principal investigators and more than 40 researchers and trainees from around the US and the world. MCRI is composed of 3 centers: the Cardiac Biology Research Center, Vascular Biology Research Center and the Center for Translational Pharmacology and Genomics.

To understand, at the molecular level, the function of the heart and vessels in health and disease.
To translate those fundamental discoveries into new strategies for diagnosis and treatment to improve cardiovascular care.
To train and mentor the next generation of cardiovascular researchers.

Improving cardiovascular health through groundbreaking research

Founded in 1997, for more than 25 years, the MCRI has made substantial advances to our understanding of the underlying pathophysiology of heart attack, high blood pressure, heart failure, arrhythmia and other cardiovascular disorders. MCRI discoveries have resulted in new drugs and devices to treat heart failure and greater understanding of how hormones effect blood vessels leading to sex differences in heart disease. Ongoing studies include investigations of novel mechanisms driving ischemic cardiovascular diseases such as angina and myocardial infarction, as well as other major cardiovascular disorders, especially hypertension, congestive heart failure, pulmonary hypertension and disorders of cardiac electrophysiology.

Leadership

MCRI is led by Executive Director Iris Jaffe, MD, PhD, a vascular biologist and cardiologist and Assistant Director Robert Blanton, MD, a cardiac biologist and cardiologist.

Contact info

Molecular Cardiology Research Institute

mcri@tuftsmedicalcenter.org

25+ years of scientific discovery

For the past 25 years, MCRI investigators and research teams have translated basic findings into new clinical strategies for the diagnosis and treatment of cardiovascular disease.

Discoveries: 1998-2018

(1998) Blood vessels respond directly to hormones. MCRI Investigators first discovered in the 1990s that the heart and blood vessels have molecular receptors needed to respond to the hormone estrogen. This discovery pioneered the field of estrogen action on the cardiovascular system and is leading to safer and more effective hormone therapies for women's heart health.
(2002) MCRI investigators have made substantial advances in understanding how the blood vessel and the platelet interact to prevent blood clotting in the healthy vessel and lead to blood clotting when the vessel is diseased. These findings contributed to our current understanding of the cause of heart attacks and strokes and are being translated into new treatments.
(2003-2018) Multiple MCRI Investigators spanning 2 decades have made substantial contributions to our understanding of the mechanisms leading to the number one cause of hospitalization – heart failure. These discoveries identified multiple new drug targets that are being developed for heart failure treatment and a discovery that white blood cells contribute to heart failure and may provide a potential new strategy to improve the heart function in the failing heart.
(2004) Blood vessel constriction can directly cause high blood pressure. Previously, high blood pressure was thought to be exclusively a kidney problem. However, in the early 2000s, MCRI investigators made several ground-breaking discoveries demonstrating that it can result from a primary defect in blood vessel function, leading to new targets for blood pressure control.
(2006/2017) MCRI efforts to understand how cancer therapy causes heart and vascular disease are leading to safer treatments for cancer patients. Work in the mid-2000s explored how cancer therapy causes heart failure. Recent studies are uncovering how the new targeted cancer treatments cause blood vessel dysfunction, leading to heart attacks and strokes, and how to prevent those adverse outcomes in cancer survivors.
(2008/2016) Small noncoding RNAs play key role in blood vessel function and contribute to hypertension as we age: In 2008, MCRI investigators discovered how microRNAs mature in blood vessel cells and can regulate blood vessel function. In 2016, one of these microRNAs was identified as contributing to blood vessel constriction with aging. High blood pressure affects 80 percent of people over the age of 80. MicroRNA levels in the serum of older people are now being evaluated as biomarkers to tailor high blood pressure treatment.
(2013) MCRI Investigators recently discovered that, in the setting of a heart attack with a blocked coronary artery, reducing the work of the heart by unloading it with a pump while delaying opening the heart artery activates a heart protection program and reduces heart attack size. This paradigm-shifting approach is now being tested in a multicenter clinical trial in people having heart attacks.
(2016) Establishment of the MCRI biobank is allowing MCRI investigators to advance our understanding of heart and blood vessel disease by working with the physicians that care for unique patient populations. For example, by studying tissue, blood samples, and DNA from the large population of patients treated at Tufts Medical Center with hypertrophic cardiomyopathy, MCRI investigators have identified new genes that modify the severity of heart disease in patients with this genetic condition.
(2017) MCRI investigators are working with engineers and biotechnology companies to develop better devices and drugs to treat heart failure. Drugs are being tested in the MCRI animal physiology core that may improve heart-pumping function and decrease heart scarring to alleviate heart failure. MCRI inventions also recently lead to the formation of a company to develop novel heart failure devices.
(2018) Obesity is a growing epidemic and contributes to blood vessel disease that leads to heart attacks and strokes. Investigators in the MCRI recently discovered that female and male blood vessels respond to obesity in completely different ways. The cause of the blood vessel dysfunction depended not only on the sex but also whether there was high blood sugar or high cholesterol along with obesity. This suggests that treatments to prevent the adverse effects of the obesity epidemic may need to be personalized based on sex as well as other risk factors in each individual patient.
- Research conducted by MCRI investigators on the ways in which hormones like estrogen act directly on the blood vessels and heart have altered how scientists and clinicians think about and design hormone replacement therapies and has led to new approaches in the pharmaceutical industry to develop more effective and safer approaches to medicines for women's health.
- Investigators within the MCRI recently identified a protein called striatin that plays a key role in allowing the estrogen receptor to interact with and bind to other proteins that mediate the effects of estrogen in cells in the blood vessel and other tissues.
- MCRI investigators have been studying how blood vessels relax and contract for nearly 20 years. MCRI investigators have discovered several important mechanisms of vascular smooth muscle relaxation in response to nitrovasodilators. These mechanisms involve, in many cases, a critical molecule that regulates vessel tone, called cyclic GMP-dependent protein Kinase I (PKGI). New drugs will likely be developed using information about PKGI in blood vessels.
- MCRI researchers discovered a new regulatory molecule for blood vessel relaxation, called Myosin Phosphatase-rho Interacting Protein (M-RIP), which has at least two important targeting functions. It localizes the myosin phosphatase complex to the actinomyosin contractile complex to dephosphorylate myosin, and it links the RhoA/ROCK pathway with myosin phosphatase, allowing RhoA/ROCK to inhibit myosin phosphatase activity in response to vasoconstrictors.
- Researchers within the MCRI have discovered that a specific class of protein hormones, named BMPs, prevents smooth muscle cells from growing too much and losing their ability to regulate blood pressure. This work continues with a study of the requirement of BMPs for the maintenance of vascular smooth cell function and the molecular mechanism by which BMPs act.
- Recent studies have implicated a potential role of Toll-like receptors (TLRs), receptors that are expressed by immune cells and activated by microbial products, in the pathogenesis of atherosclerosis. MCRI researchers have shown that vascular smooth muscle cells also express several TLRs, and that activation of these receptors upon exposure to microbial products elicits dramatic changes in smooth muscle cell phenotype, including cell proliferation and synthesis of chemokines, phenotypic changes similar to those that contribute to vascular disease.

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