INTERNATIONAL COENZYME Q10 ASSOCIATION

Want to dive deeper into the data? Check out the full open-access study by Meza-Torres et al. (2025) in Antioxidants: www.mdpi.com/2076-3921/14....
A must-read for anyone interested in CoQ biology, aging, and mitochondrial resilience. #OpenScience #CoenzymeQ

Takeaway: Aging erodes our CoQ factories; exercise can shore them up, resveratrol helps a bit, but effect depends on tissue. Future therapies could target Coq gene regulation directly. Thoughts on translation to humans?

This work lays a foundation for therapeutic strategies focused on enhancing endogenous CoQ production—via transcriptional and lifestyle modulation—rather than relying solely on supplements.

The authors suggest combining lifestyle (exercise) with nutraceuticals (resveratrol or other modulators) could best preserve CoQ biosynthesis with age, delaying mitochondrial dysfunction and oxidative damage.

Exercise appears as a more robust stimulus for CoQ gene network maintenance—especially in high-energy tissues like muscle and heart. Resveratrol adds benefit but is less potent.

Why is this important? CoQ is central to OXPHOS and antioxidant defense. Its decline may contribute to age-related loss of mitochondrial resilience, higher oxidative stress, and decline in organ function.

The study emphasizes that supporting CoQ-synthome expression is crucial—not all benefits come from supplementing CoQ externally. Building intrinsic machinery matters.

Interestingly, brain and kidney were less responsive to both interventions. This hints at tissue-specific regulation of CoQ biosynthesis and perhaps limited reversibility in certain organs.

Exercise training upregulated several Coq genes in muscle and heart—more consistently than resveratrol—and boosted CoQ levels where gene expression increased, especially in cardiac tissue.

Resveratrol (in drinking water) partially restored Coq transcripts in muscle and liver—but effects were tissue-specific and modest. Transcriptional rescue didn’t always translate to higher CoQ levels.

Result: most Coq genes decline steadily with age—especially in muscle and brain—mirroring drops in CoQ content. This suggests aging impairs CoQ-synthome integrity, reducing CoQ supply and cellular antioxidant capacity.

They measured transcripts of Coq genes (Coq2–Coq9) in skeletal muscle, heart, liver, kidney, and brain—from young to old mice—while also measuring CoQ9 and CoQ10 levels in each tissue.

What happens to coenzyme Q (CoQ) production machinery in aging tissues—and can resveratrol or exercise reset it? Meza Torres et al. tracked expression of the “CoQ synthome” and CoQ levels in mice across ages and interventions.⬇️

RTN4IP1 is no longer a black box. With collaborative science, we’re piecing together the puzzle of mitochondrial disease—one gene at a time. What other secrets do our mitochondria hold? 🔬✨

#Genetics #Mitochondria #CRISPR #Science #RTN4IP1 #CoenzymeQ #LeighSyndrome

It also shows why time matters in biology. Signals lost in noise become patterns when viewed over time. In mitochondrial science, that’s a game changer. 🔑📊

This work has real-world impact: it can improve diagnostics for rare disorders, uncover hidden disease mechanisms, and eventually support tailored therapies. 🏥🧬

Their time-resolved approach didn’t just catch essential genes—it captured regulators and assembly factors with subtle effects that traditional screens would miss. A dynamic roadmap of mitochondrial function! 🗺️

Another gene, ECHS1, was also flagged. Though known for fatty acid metabolism, it turns out ECHS1 regulates mitochondrial function independently, affecting key enzymes like pyruvate dehydrogenase. 🧠🧪

Proteomics revealed a dramatic loss of complex I and other OXPHOS proteins in RTN4IP1-deficient cells. It’s like removing the conductor from an energy orchestra. 🎻🎼

Without RTN4IP1, complex I activity vanishes and oxygen consumption in mitochondria drops sharply. The cells simply can’t survive under mitochondrial stress conditions. 💀

This builds on earlier work by Isaac Park et al. (2023), who showed that RTN4IP1 is a mitochondrial oxidoreductase required for CoQ synthesis—a key electron shuttle in the respiratory chain. 🧪

One standout hit was RTN4IP1. Previously a mystery, this gene turned out to be essential for mitochondrial respiration and the full assembly of complex I—the first link in the respiratory chain. 🔧🧬

nlike previous screens, they tracked changes over time using galactose media. Why? Because cells lacking OXPHOS function can’t survive on galactose—it forces them to rely solely on mitochondria. ⏳🧪

Zamora-Dorta and colleagues built a custom CRISPR library targeting nuclear-encoded mitochondrial genes. Their goal? Find new regulators of OXPHOS—not just the usual suspects. 🧬🔍

Mitochondrial disorders often stem from disruptions in oxidative phosphorylation (OXPHOS). While core OXPHOS components are well-studied, many regulatory and assembly factors remain poorly understood—and may hold the key to unsolved CoQ-related pathologies. 🧬⚙️

Did you know a little-known gene might be key to understanding severe mitochondrial diseases like Leigh syndrome? A new study sheds light on RTN4IP1 and its crucial role in cellular energy. Let’s dive in. 👇

Latest Research and news on CoQ! - International Coenzyme Q10 Association Stay up to date with the latest research and discoveries on Coenzyme Q (CoQ10), from mitochondrial function to emerging therapies.

The ICQ10A starts today our new section as newsletter with the newest information about research in #coenzymeQ from basics to clinical aspects.
In this first number five new recent publications are resumed.

Latest Research and news on CoQ! icq10a.com/latest-resea...

📝 Master Class by Franklin L. Rosenfeldt (Swinburne Univ. & Baker Institute), vice-chairman of the @icq10a.bsky.social until yesterday: Writing a scientific paper isn’t just for experts—it's a skill anyone can learn. Here's how to get published without losing your mind. 🧵 #11thConferenceICQ10A

CoQ10 could be more than a supplement. With the right drugs, we might help the body recycle and retain it better—opening new paths for treating mitochondrial diseases.

CoQ10 could be more than a supplement. With the right drugs, we might help the body recycle and retain it better—opening new paths for treating mitochondrial diseases.