Chris Newton-Cheh is a heart failure cardiologist and human geneticist.  The Newton-Cheh lab studies the genetic basis of cardiovascular traits and disease, follows up genetic leads to identify previously unsuspected disease mechanisms, and tests the impact of genetics on response to drugs and environment.  We are leveraging the rapid growth of human genetics to identify genetic variants that underlie hypertension, heart failure and arrhythmias, to translate genetic discoveries into an improved understanding of human physiology through clinically-focused research, and to define the role of genetics and other factors in predicting patients’ risk of disease and likelihood of a beneficial or toxic response to drug therapies.

Questions being addressed in the lab

  1. What is the inherited basis of hypertension, heart failure and arrhythmias?
  2. How do human genetic variants identify novel mechanisms influencing risk of cardiovascular disease?
  3. How do genetic variants influence cardiotoxic response to medication exposure?

Projects underway to answer these questions

  1. We are actively recruiting MGH Heart Center patients to participate in the Cardiovascular Biorepository (CVBio) in collaboration with the Partners HealthCare Biobank, with the goal of identifying novel genetic factors contributing to life-threatening conditions such as dilated cardiomyopathy and arrhythmias.

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  3. We have been pursuing the molecular mechanisms by which genetic variation in atrial natriuretic peptide and the natriuretic peptide receptor influences blood pressure and risk of hypertension through cellular models.

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  5. We are actively recruiting patients who are starting medications associated with risk of sudden cardiac death due to a ventricular arrhythmia called torsade de pointes in order to determine the role that common genetic variants play in risk of this life-threatening drug toxicity.

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Answers Found

  1. We have identified scores of genes that influence blood pressure, QT interval variation and left ventricular hypertrophy (a precursor to congestive heart failure).

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  3. Human genetic variants have led us to identify several microRNAs that negatively regulate expression of atrial natriuretic peptide.

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  5. We characterized the relative effects of genetic variation and dietary and intravenous sodium challenge on ANP production in translational work in the MGH Clinical Research Center.

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