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A joint study by the University Medical Center Göttingen (UMG) and the University Hospital Würzburg 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. The findings were published in the journal Circulation Research.
Atrial fibrillation is the most common form of persistent heart rhythm disorder. According to the German Heart Foundation, around two million people in Germany are affected. The condition disrupts the heart’s electrical activity and can lead to irregular heartbeats, shortness of breath, and, over time, serious complications such as heart failure or stroke. Until now, the reasons why heart muscle cells lose their rhythm in atrial fibrillation were not fully understood.
A research team from the University Medical Center Göttingen (UMG), led by Prof. Dr. Niels Voigt, Professor of Molecular Pharmacology at the Institute of Pharmacology and Toxicology at UMG, together with the University Hospital Würzburg (UKW), led by Prof. Dr. Christoph Maack, Head of the Department of Translational Research at the German Center for Heart Failure (DZHI) at UKW, 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 the heart muscle to contract. The mitochondria use this calcium signal to produce energy, especially when the heart is under stress.
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, limiting the regeneration of key energy carriers. High-resolution microscopy further revealed that the spatial proximity between the sarcoplasmic reticulum and mitochondria is lost in diseased cells, throwing the heart muscle’s energy supply out of balance.
‘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 findings have been published in the journal Circulation Research.
Original publication:
Julius Ryan D. Pronto, et al. Impaired Atrial Mitochondrial Calcium Handling in Patients With Atrial Fibrillation. Circulation Research (2025). DOI: https://doi.org/10.1161/CIRCRESAHA.124.325658
Cholesterol-lowering drug supports calcium uptake
In their investigations, 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. Electron tomography allows cellular structures to be visualized in three dimensions down to the nanometer scale. Using this method, the researchers could precisely measure the spatial proximity between mitochondria and the sarcoplasmic reticulum. 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.
‘Our findings open new perspectives for the treatment of atrial fibrillation,’ says first author Dr. Julius Pronto, postdoctoral researcher at the Institute of Pharmacology and Toxicology at UMG. ‘If it becomes possible to specifically stabilize mitochondria and improve their calcium uptake, this could ultimately reduce the risk of heart rhythm disorders.’
Calcium in focus
In an earlier study in collaboration with the University Hospital Würzburg, the research team showed that calcium can also serve as a marker to better predict the risk of dangerous heart rhythm disturbances after heart surgery. The new study takes this a step further by highlighting the fundamental cellular mechanisms that may underlie such disorders.
Research funding
The project was financially supported by the German Center for Cardiovascular Research (DZHK), the German Research Foundation (DFG), and the Göttingen Excellence Cluster ‘Multiscale Bioimaging: From Molecular Machines to Networks of Excitable Cells’ (MBExC).
Caption - picture 1
Cover image of the current issue of ‘Circulation Research’. The image shows the regular, blue-colored arrangement of mitochondria in atrial heart muscle cells from a patient without a heart rhythm disorder. The cytoskeleton, shown in magenta, supports the cell structure and contributes to the orderly organization of the mitochondria.
Prof. Dr. Niels Voigt, Institute of Pharmacology and Toxicology, Phone +49 551 / 39-65174, niels.voigt@med.uni-goettingen.de
Julius Ryan D. Pronto, et al. Impaired Atrial Mitochondrial Calcium Handling in Patients With Atrial Fibrillation. Circulation Research (2025). DOI: https://doi.org/10.1161/CIRCRESAHA.124.325658
Caption see below the text
Copyright: circulation research
Prof. Dr. Niels Voigt, Professor of Molecular Pharmacology at the Institute of Pharmacology and Toxi ...
Copyright: mbexc/swen pförtner
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Caption see below the text
Copyright: circulation research
Prof. Dr. Niels Voigt, Professor of Molecular Pharmacology at the Institute of Pharmacology and Toxi ...
Copyright: mbexc/swen pförtner
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