We Thought This Cell Death Phenomenon Was Irreversible, But We Were Wrong

According to new research, pyroptosis, a type of apoptosis associated with infection and an inflammatory response, can indeed be stopped and managed, while the process was previously thought to be irreversible once it started.

Killing cells with myotoxin is something the body uses to stay healthy, although these methods can also be hijacked to cause harm. What makes studying cell death difficult is the inability to predict how it will start, along with the different types of effects it has in different cells and different people.

Here the research team used a new method to analyze laryngitis, creating a custom-made version of a protein associated with light-responsive cell death. Laboratory experiments have revealed signs of a dynamically degrading autoregulation in response to external conditions.

“He showed us this form of cell death is not a one-way ticket,” says pharmacologist Gary Mo of the University of Illinois at Chicago. “The process is actually programmed with a cancel button, an off switch.”

The protein created for the study was an optical (light-responsive) version of gasdermine, which is key to the biochemical reactions that make up hyperacidity. It opens large pores in the cell membranes to kill them on instructions from the body.

By using fluorescent imaging technology to precisely activate custom gasdermine, the researchers can see that under certain conditions — such as a certain concentration of calcium ions, for example — the open pores close again in seconds.

While it is still early days in terms of knowing why this happened and the exact conditions that led to it, it is evidence that acidity can start and then stop again depending on what is happening around it.

“The optogenetic gas allowed us to bypass the pathogen’s unexpected behavior and altered cellular response because at the molecular level it mimics what happens in the cell once the epididymal inflammation begins,” says Mo.

Many diseases, including some types of cancer, are caused by malfunctions in cell death processes that do not work as they should. This imbalance can also cause inflammation to get out of control after an infection – as with sepsis, for example.

Improved knowledge of how cell death works—and kinetotoxicity is one of the main types—could improve treatments too, if we are able to find ways to control which cells are killed and when.

Previous research has revealed the ways in which bacteria can avoid episodes of cell proliferation and apoptosis (another type of cell death), and as pathogens get smarter, it’s important that we continue to get drugs to beat them.

“Understanding how to control this process opens up new avenues for drug discovery, and now we can find drugs that work for both sides,” Mo says.

“It allows us to think about regulating, either enhancing or limiting, this kind of cell death in diseases where previously we could only remove this important process.”

The search was published in Nature Communications.


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