Lai-Hua Xie
Rutgers University-New Brunswick, NJ·Physiology
Too much iron can poison the heart. Iron builds up in heart muscle in people with the genetic disorder hereditary hemochromatosis and in patients needing repeated transfusions for sickle cell anemia or beta thalassemia, and the resulting iron overload cardiomyopathy, a weakened heart muscle, is a major cause of death.
- Fields
Physiology
Medicine & Clinical Research
Pharmacology
- Topics
ferroptosis
iron overload cardiomyopathy
ischemia-reperfusion injury
- Grants
- 1 known grant, through Nov 2026
What they work on
- Determine whether the mitochondrial calcium uniporter (mCU), a channel admitting calcium into mitochondria, also carries iron into heart-cell mitochondria and drives calcium dysregulation, oxidative stress and iron-induced cardiac toxicity, in isolated myocytes and in vivo.
- Test how iron's direct activation of TRPC ion channels relates to cardiac dysfunction, both acutely in isolated cells and in animals with iron-induced cardiomyopathy.
- Populate a computer model of excitation–contraction–mitochondria coupling with the experimental data and simulate how iron alters the electrical, contractile and mitochondrial behavior of heart cells.
- Map ferroptosis pathways in Duchenne muscular dystrophy hearts by profiling related genes, proteins and biomarkers, testing sensitivity to ferroptosis inducers, and attempting to lessen cardiomyopathy by inhibiting ferroptosis in vivo.
- Identify protective anti-ferroptosis mechanisms in woodchucks, which resist ischemia-reperfusion injury, through in vitro and in vivo studies.
More about the research
Iron levels also rise in the hearts of Duchenne muscular dystrophy (DMD) mouse models, and in hearts after ischemia-reperfusion, when blood flow is cut off and then restored as in a heart attack. How iron damages the heart is unclear. This project proposes that iron and calcium act together to create a toxic environment that kills heart cells through ferroptosis, an iron-dependent form of cell death.
Why it matters
Iron overload cardiomyopathy kills patients with hemochromatosis and with transfusion-dependent sickle cell anemia or beta thalassemia, and cardiomyopathy affects most people with Duchenne muscular dystrophy. By identifying how iron and calcium together trigger ferroptosis in the heart, this work could point to treatment or prevention targets for these conditions and for the reperfusion injury and myocardial stunning that follow a heart attack.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Bround
Baylor College of Medicine, TX·Physiology·Early-career
Determine whether LETM1 drives proton/calcium exchange in heart mitochondria, using mice in which Letm1 is deleted from the heart to study heart function, mitochondrial function and how charged particles cross the mitochondrial membrane.
Shey-Shing Sheu
Thomas Jefferson University, PA·Physiology
Test whether hypertrophic stress raises levels of mitochondrial ryanodine receptor type 1 (mRyR1), a calcium channel, to boost mitochondrial calcium uptake and ATP production, using RyR1-overexpressing and other mouse models.
Ming-Feng Tsai
University of Virginia, VA·Biophysics
Establish how MICU3, a neuron-specific subunit of the mitochondrial calcium uniporter, boosts the channel's calcium uptake, using biochemical, electrophysiological and structural methods.
The school
Rutgers University-New Brunswick: 57 labs on PI Pages, $837M a year on research, 713 research doctorates a year.
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