Treating Heart Failure by Targeting a Mitochondrial Protein


Heart Failure: A pathophysiologic condition in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate adequate with metabolic requirements of the tissues.
Recent Advancements in Heart Failure:

Treating Heart Failure by Targeting a Mitochondrial Protein
A new researchers study shows how one mitochondrial protein (FUNDC1), is connected to heart dysfunction and heart failure. This research shows unique explanation for how heart failure develops and goes all the way to the miniscule organelles inside individual cells.
FUNDC1 is an outer mitochondrial membrane protein whose function has yet to be entirely explained. What scientists from the current study do know, though, is that reducing its levels in heart muscle cells, called cardiomyocytes, initiates cardiac dysfunction and makes existing dysfunction worse.
Additionally, intervention between FUNDC1’s interaction with certain protein receptors blocks the release of calcium from an organelle called the endoplasmic reticulum (ER), preventing calcium from reaching the mitochondria. This leads to a plethora of problems stemming from mitochondrial and cardiac dysfunction, ultimately resulting in heart failure.
The formation of MAMs (mitochondria-associated ER membranes) mediated by the FUNDC1 was consequentially suppressed in heart failure patients, which provides evidence that FUNDC1 and MAMs actively participate in the development of heart failure.
Join us at 28th International Conference on Cardiology and Healthcare (Cardiology Care 2018) held during august 9-11, 2018 in Abu Dhabi, UAE for more recent updates in cardiology research.
For details contact:
Aurora Lorenz
Program Manager-Cardiology Care 2018
Direct: +1 (702) 508-5200 Ext: 8122
Tel: +1 (800) 216 6499

Mail:
cardiology@healthconferences.org

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