Disrupted calcium signaling can throw the heart off rhythm (Zetia)

A study provides new insights into why heart muscle cells lose their rhythm in atrial fibrillation. Disrupted calcium signaling between key cellular structures in the heart may be a critical underlying mechanism.

A research team has now uncovered new evidence suggesting that disrupted communication between key cellular structures in heart muscle cells plays a critical role in the development of this rhythm disorder.

The research focuses on mitochondria—the "powerhouses of the cell"—and the sarcoplasmic reticulum, a fine network of tubules within heart muscle cells that stores calcium and releases it with each heartbeat. This calcium is what triggers heart muscle to contract. The mitochondria use this calcium signal to produce energy.

Normally, the sarcoplasmic reticulum and mitochondria are tightly coupled. In patients with atrial fibrillation, however, this coupling appears to be disrupted. The team showed that mitochondrial calcium uptake is reduced in atrial fibrillation.

"We suspect that the loss of calcium communication contributes to the electrical instability of the heart muscle and is therefore a central mechanism underlying the rhythm disorder," explain Prof. Voigt and Prof. Maack.

The team analyzed heart muscle samples from patients with and without atrial fibrillation. In addition to biochemical measurements, they used high-resolution imaging techniques such as electron tomography and STED nanoscopy.

STED nanoscopy (Stimulated Emission Depletion Microscopy) provided an even higher resolution than conventional light microscopy, revealing the fine structure of the cells. These techniques showed that in atrial fibrillation, mitochondria lose their organized structure and detach from the sarcoplasmic reticulum.

The research groups also investigated whether the impaired heart function could be influenced—and found a surprising result: an already approved cholesterol-lowering drug was able to partially restore mitochondrial calcium uptake in heart muscle cells. An analysis of patient data further revealed that people taking this medication were less likely to develop atrial fibrillation.

Message from Jim Robinson:

Dear FRiends,

We need your continuing support to keep FR funded. Your donations are our sole source of funding. No sugar daddies, no advertisers, no paid memberships, no commercial sales, no gimmicks, no tax subsidies. No spam, no pop-ups, no ad trackers.

If you enjoy using FR and agree it's a worthwhile endeavor, please consider making a contribution today:

Click here: to donate by Credit Card

Or here: to donate by PayPal

Or by mail to: Free Republic, LLC - PO Box 9771 - Fresno, CA 93794

Thank you very much and God bless you,

Jim

The writeup skips the drug that helps, and it also doesn’t mention another antioxidant that can help, but is hard to find.

The drug is Ezetimibe (Zetia) and the antioxidant is MitoTEMPO.

MitoQ and ergothioneine can help mitochondria with oxidation, similar to what I read about MitoTEMPO. Also, urolithin A can help regenerate defective mitochondria. However, these other supplements were not mentioned as tested.

The “Take Charge Of Your Health” Ping List
This high volume ping list is for health articles and studies which describe something you or your doctor, when informed, may be able to immediately implement for your benefit.

Email me to get on either the “Common/Top Issues” (20 - 25% fewer pings) or “Everything” list.

Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.