A way has been found to protect mitochondria from destruction

Mitochondria are vital elements inside every cell, producing energy from nutrients. When a person is stressed, especially at the cellular level, these mini power plants become vulnerable: their structure breaks down and they cease to fulfil their functions. Such a breakdown can cause or exacerbate dozens of serious diseases, including neurodegenerative disorders and inflammation. American researchers have discovered a vulnerability in the protein that causes mitochondria to break down under stress.

A way has been found to protect mitochondria from destruction

This is exactly the problem that experts from SLAC National Laboratory and Stanford University have tried to solve. The team focused on the destructive effects of hydrogen peroxide, an active molecule that provokes stress inside cells. They set out to find a way to protect mitochondria and stop them from being destroyed.

The key finding was a small molecular agent called SP11. Its addition to human cells with already damaged mitochondria gave an impressive effect – the destroyed structures recovered and began to produce energy again. The study has been published in the journal Nature Communications, and the molecule itself has already been patented for possible drug development.

Professor Daria Mohly-Rosen, who led the project, notes: ‘If we can learn how to keep mitochondria in working order, we can improve conditions in a multitude of chronic diseases.’ Her words are not unsubstantiated – she has previously been involved in the development of drugs successfully used in medicine.

Although mitochondria are most often cited as a source of cellular energy, they also perform other important functions: synthesising molecular building blocks and ‘switching off’ damaged cells, preventing mutations and inflammation. Moreover, it has recently been shown that mitochondria can even transfer from one cell to another, passing on both benefits and harms.

The molecular malfunction that triggers mitochondrial destruction is caused by the Fis1 protein, which under conditions of stress and oxidative damage begins to interact with the wrong ‘partners’. In normal mitochondrial fission is carefully regulated, but under the influence of Fis1 process becomes chaotic – mitochondria fall apart into useless debris, unable to provide the cell with energy.

The researchers spent more than three years looking for the Achilles’ heel of Fis1. Using computer modelling, X-ray crystallography and experiments, they discovered that Fis1 has a site – the amino acid Cys41 – that becomes vulnerable during cellular stress. This is where SP11 attaches, blocking further degradation.

SP11 includes a chemical backbone already used in drugs for nausea, allergies and mental disorders. This suggests that the path to making SP11 into an effective drug could be relatively short – if its safety and efficacy are confirmed in new clinical trials.

In the future, SP11 could be the basis for drugs that protect mitochondria in patients with Parkinson’s disease, diabetes, heart failure, inflammatory bowel disease and many other ailments. Attention to mitochondria as a starting point for many pathologies is one of the most promising areas of modern medicine.

Published

May, 2025

Duration of reading

3-4 minutes

Category

Science

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