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The Laboratory of Dr. Brian Jensen


  • Wei Huang – (919)843-4217

Location: 2nd floor Medical Biomolecular Research Building

The overarching focus of the Jensen lab is the explication of the pathobiology of heart failure. We currently are pursuing three distinct but related avenues of investigation.

1.    Metabolic mechanisms of cardioprotection through alpha-1A adrenergic receptor activation: Heart failure (HF) is characterized by markedly elevated levels of catecholamines that bind to adrenergic receptors (ARs) in the heart. The toxic effects of excessive beta (β)-AR stimulation are well described, and drugs that block β-ARs are cornerstones of contemporary HF therapy.  Cardiac alpha (α)1-ARs have received less attention, however data from cell and animal studies indicate that they protect against the development of HF. There are two α1-AR subtypes in the heart: α1A, and α1B.  The α1B mediates cardiac hypertrophy induced by non-selective α1-AR agonists like phenylephrine. Activation of the α1A protects against cardiomyocyte death and increases contractility in the failing heart, though the mechanisms underlying these adaptive effects are incompletely understood. We recently showed that an oral selective α1A agonist drug, dabuzalgron, preserves ATP content and mitochondrial function in mouse HF models. Collectively, our ongoing work challenges the prevailing paradigm that chronic catecholamine surge exerts uniformly deleterious effects in the failing heart.

2.    Kinase inhibitor cardiotoxicity: In collaboration with Gary Johnson in the Department of Pharmacology, we are investigating the surprising cardiotoxicity of new anti-cancer drugs, kinase inhibitors.  We have shown that kinase inhibitor-induced cardiac injury arises as a result of both on- and off- target effects, may of which affect cardiomyocyte metabolism.  We hope this work will lead to the development of a platform for predicting cardiotoxicity of novel kinase inhibitors before they reach broad clinical use.

3.    A novel role for the nuclear receptor RORα in regulating cardiac hypertrophy: JuYoun Beak, a postdoctoral fellow in the lab, brought expertise in orphan nuclear receptors gained from her time in the Anton Jetten lab at NIEHS. Dr. Beak discovered that the orphan nuclear receptor, RORα, is expressed in the mouse and human heart and mediates cardiac hypertrophy in response to angiotensin II.  In collaboration with Dr. Jetten, we are investigating the mechanisms underlying this exciting novel finding.

View Dr. Jensen’s publications on PubMed.