Completed Cells, Biochemistry & Physiology Genetics & Molecular Biology

CEROX-miRNA Control of Mitochondrial OXPHOS Activities in Health and Disease.

In plain English

AI plain-English summary

Every cell in the body relies on tiny power plants called mitochondria to generate energy, and this project aims to control that energy output by manipulating specific RNA molecules that act as genetic dimmer switches. Mitochondrial dysfunction is linked to a wide range of human diseases, from rare genetic disorders to common conditions like diabetes and neurodegeneration. Researchers know that certain long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) form competing networks—called CEROX networks—that regulate mitochondrial activity. But it remains unclear exactly which RNAs are involved, how these networks differ between tissues, and whether they can be deliberately tweaked to boost or reduce energy production. This project will map these RNA networks across different cell types, then test whether disrupting them can alter mitochondrial enzyme activity in living cells and animal models. If successful, it could open a new route for treating diseases where mitochondria are underperforming—by using drugs that inhibit a specific microRNA or boost a particular lncRNA to restore energy levels in only the affected tissue, avoiding side effects elsewhere. This is fundamental science: it asks how cells naturally control their energy supply. While no immediate medical application exists, understanding these RNA control circuits could eventually lead to therapies for conditions as varied as muscle wasting, heart failure, and metabolic disorders.

View original technical description
Improving mitochondrial energy production in disease-relevant cells by modulating noncoding RNAs - What long noncoding RNAs (lncRNAs) and micro-RNAs (miRNAs) control mitochondrial enzymatic activity via crosstalking networks? - How do these dynamic networks of CEROX (competitive endogenous regulator of oxidative phosphorylation) transcripts and miRNAs vary among tissues and cells? - By perturbing these networks in vitro and in vivo, what is the extent to which mitochondrial oxidative phosphor ylation (OXPHOS) enzymatic activities can either be boosted or reduced? - Can symptoms of the many human diseases associated with mitochondrial dysfunction be ameliorated by perturbing a CEROX-microRNA network that is tissue- or cell type-specific? - Can this be achieved by inhibiting microRNA or by boosting lncRNA expression?

View the original record at the funder ↗

Researchers

Chris Ponting (EPMC Awardee)

Related Research

Grants with similar aims, by meaning.

Lipid mediated organelle-crosstalk controls cell-fate and function
The Mitochondrial End Game : How key proteins control more than just translation termination
Investigating the relationship between respiratory chain organisation and mitochondrial morphology by electron cryo-tomography
Regulation of mitochondrial expression
Form and Function of the Mitochondrial Retrograde Response

Original classification

Investigator Award in Science

Plain English summaries and category classifications on this site are generated by AI and may not perfectly reflect the original research.