Magnesium is a vital mineral that plays a key role in numerous biological processes in the body. Among other functions, it is crucial for the mitochondria—the power plants of our cells—to produce and utilize ATP, the body’s primary energy molecule.
When mitochondrial function is impaired, a wide range of symptoms can arise, sometimes affecting a single organ but more often manifesting in multiple organs or systems simultaneously.
In a study published in Nature Structural & Molecular Biology, researchers reveal how mitochondria receive precisely the right amount of magnesium they require.
How magnesium channels work
Mitochondria are surrounded by a membrane containing ion channels that act like gate with locks, allowing specific substances to pass through. For magnesium to enter, these channels must open or close at just the right time.
“If there’s too little magnesium in the mitochondria, the channel opens, and magnesium flows in from the outside. What’s remarkable is that the process regulates itself almost instantaneously. Sensors inside the mitochondria detect when there’s enough magnesium, prompting the channel to close, or when more is needed, triggering it to reopen,” explains Pontus Gourdon, lead researcher at Lund University.
To uncover the mechanisms of these magnesium channels, the researchers employed advanced cryo-electron microscopy techniques, a Nobel Prize-winning technique that allows scientists to observe molecular structures with incredible detail. The magnesium channel is less than a thousandth the width of a human hair, yet the technology enables researchers to view its 3D structure.
“By understanding the structures of these proteins, we gain insight into how these channels work at the molecular level—how magnesium flows under specific conditions but not others,” Gourdon adds.
Fundamental research with far-reaching potential
This study is a testament to the power of fundamenta research, which lays the groundwork for solving complex problems. For instance, the discovery of DNA’s structure in the 1950s—another triumph of basic research—paved the way for advancements in genetic engineering and modern medicine.
The findings from this study could potentially be applied to develop tools that influence how these channels function. Gourdon envisions the possibility of designing inhibitors to bind to similar bacterial channels and keep them closed, or even “freezing” the channels in their open state to boost magnesium intake when needed.
“I hope our results will not only improve our understanding of mitochondria function but also provide new insights into the origins and treatment of mitochondrial diseases,” says Gourdon.