Mitochondrial Protein in Cardiac Muscle Cells Linked to Heart Failure, Study Finds


Source: Georgia State University

Summary: Researchers in a new study found that when a mitochondrial protein of the cardiac muscle cells is reduced, initiates cardiac dysfunction and heart failure.


Mitochondria (cell organelles – generally called as a powerhouse of the cell) has numerous functions in the body such as energy production, generates reactive oxygen species and also signal transduction. As the myocardium (muscular wall) of the heart is a high-energy-demand tissue, mitochondria play a key role in maintaining optimal cardiac performance. Researchers from the Georgia State University in a new study found that when an outer mitochondrial membrane protein, FUN14 with domain 1 (FUNDC1) of the cardiac muscle cells is reduced, initiates cardiac dysfunction. Also, disrupting how FUNDC1, when binds to a specific receptor, inhibits the release of calcium from the endoplasmic reticulum (ER), into the mitochondria of these cells and result in mitochondrial dysfunction, cardiac dysfunction and heart failure. The research findings were published in the journal Circulation.

Reduced Mitochondrial protein result in heart disease

Credit: Georgia State University

In the body, mitochondria and ER are interconnected to form their own endomembrane networks. These mitochondria-ER junctions are called as mitochondria-associated ER membranes (MAM) – play a key role in regulating the calcium transfer between ER and mitochondria. The dysfunctional MAMs result in neuronal disorders which include Alzheimer’s disease and Parkinson’s disease but their role in cardiac pathologies is not well understood until now. This study provided an evidence that FUNDC1 and MAMs actively participate in the development of heart failure, a finding that could provide insight for new treatments for cardiovascular diseases.

Dr. Ming-Hui Zou said, “Our study found the formation of MAMs mediated by the mitochondrial membrane protein FUNDC1 was significantly suppressed in patients with heart failure, which provides evidence that FUNDC1 and MAMs actively participate in the development of heart failure” and further added,  “This work has important clinical implications and provides support that restoring proper function of MAMs may be a novel target for treating heart failure.”


More Information: Shengnan Wu et al, “Cardiac Fundc1 Ablation Protects Diabetic Cardiomyopathy”, Circulation (2017). http://circ.ahajournals.org/content/136/Suppl_1/A18819


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