CoQ10 protecting lung and liver cells from methotrexate damage

CoQ10: Your Cellular Shield Against Fibrosis?

Rhea Morgan in Health & Wellness December 2025 • 4 min read.

"Unlocking the Potential of Coenzyme Q10 in Protecting Your Lungs and Liver from Methotrexate Damage."

Methotrexate, a widely used medication for cancer and autoimmune diseases, can sometimes cause serious side effects, including lung and liver fibrosis. Fibrosis occurs when these organs develop scar tissue, impairing their function. This can be a major concern for individuals undergoing methotrexate treatment, and many are seeking ways to mitigate these risks.

Emerging research suggests that Coenzyme Q10 (CoQ10), a naturally occurring antioxidant, may offer a protective effect against methotrexate-induced fibrosis. Scientists are exploring CoQ10's potential to modulate autophagy, a cellular process that helps clear out damaged components and maintain healthy tissue function. By supporting autophagy, CoQ10 could potentially reduce the severity of fibrosis in the lungs and liver.

This article delves into a recent study investigating the effects of CoQ10 on rats treated with methotrexate. We'll break down the key findings, explore how CoQ10 appears to work at a cellular level, and discuss the implications for individuals concerned about methotrexate-related side effects. Discover how this readily available supplement may offer a proactive approach to supporting your lung and liver health.

How CoQ10 Fights Fibrosis: Activating Your Cellular Cleanup Crew

CoQ10 protecting lung and liver cells from methotrexate damage

The study's findings suggest CoQ10's protective effects stem from its ability to influence autophagy, a critical process where cells remove damaged components to stay healthy. Researchers found that methotrexate disrupted autophagy in the rats' lung and liver tissue. However, when CoQ10 was administered alongside methotrexate, the autophagy process appeared to be reactivated.

Here's a breakdown of the key cellular players involved and how CoQ10 seems to make a difference:

mTOR: Methotrexate increased the expression of mTOR, a protein that inhibits autophagy. CoQ10 helped to bring mTOR levels down, allowing autophagy to proceed.
MAP1LC3B and p62/SQSTM1: These are markers of autophagy. Methotrexate decreased their levels, indicating reduced autophagy. CoQ10 reversed this effect, boosting the presence of these markers and promoting cellular cleanup.
HMGB1: This protein is linked to inflammation and fibrosis. Methotrexate increased HMGB1 levels in the lung and liver, while CoQ10 helped to lower them.

In addition to its effects on autophagy, CoQ10 also acted as an antioxidant, reducing oxidative stress in the lung and liver tissue. Oxidative stress is a key contributor to fibrosis, so CoQ10's antioxidant properties likely contribute to its protective effects.

CoQ10: A Promising Complement, Not a Replacement

The study offers encouraging evidence for CoQ10's potential to mitigate methotrexate-induced lung and liver fibrosis. By modulating autophagy, reducing oxidative stress, and lowering HMGB1 levels, CoQ10 appears to target multiple pathways involved in the development of fibrosis.

However, it's important to remember that this research was conducted on rats, and more studies are needed to confirm these findings in humans. Additionally, CoQ10 should not be considered a replacement for conventional medical treatment. If you are taking methotrexate, it's crucial to consult with your doctor before starting any new supplements, including CoQ10.

With that said, CoQ10 may be a valuable addition to a comprehensive strategy for protecting your lung and liver health while undergoing methotrexate treatment. By discussing this research with your healthcare provider, you can make informed decisions about how to best support your well-being.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1016/j.biopha.2018.10.133, Alternate LINK

Title: Coenzyme Q10 Attenuates Lung And Liver Fibrosis Via Modulation Of Autophagy In Methotrexate Treated Rat

Subject: Pharmacology

Journal: Biomedicine & Pharmacotherapy

Publisher: Elsevier BV

Authors: Doaa I. Mohamed, Eman Khairy, Sherin Shafik Tawfek, Eman K. Habib, Marwa A. Fetouh

Published: 2019-01-01

Everything You Need To Know

What is CoQ10 and how does it work to protect against fibrosis?

Coenzyme Q10 (CoQ10) is a naturally occurring antioxidant that has shown promise in mitigating methotrexate-induced fibrosis. It works by modulating autophagy, a cellular process where cells remove damaged components. CoQ10 also acts as an antioxidant, reducing oxidative stress, which is a key factor in fibrosis development. Specifically, CoQ10 influences key cellular players like mTOR, MAP1LC3B, p62/SQSTM1, and HMGB1, thereby offering a potential protective effect against lung and liver fibrosis.

What is the role of Methotrexate and what are the associated risks?

Methotrexate is a medication used for cancer and autoimmune diseases. A significant side effect of Methotrexate can be lung and liver fibrosis. Fibrosis is the formation of scar tissue in these organs, which impairs their function. This can be a major concern for individuals undergoing Methotrexate treatment, highlighting the importance of finding ways to mitigate these risks.

How does CoQ10 specifically interact with cellular processes to combat fibrosis?

The study suggests CoQ10's protective effects stem from its ability to influence autophagy. Methotrexate disrupts autophagy, and CoQ10 can help reactivate it. CoQ10 impacts several cellular players. Methotrexate increases mTOR, inhibiting autophagy, while CoQ10 helps lower mTOR levels, allowing autophagy to proceed. Methotrexate decreases MAP1LC3B and p62/SQSTM1, markers of autophagy, but CoQ10 reverses this effect. Methotrexate increases HMGB1, linked to inflammation and fibrosis, and CoQ10 helps lower these levels. Additionally, CoQ10 acts as an antioxidant, reducing oxidative stress, a key contributor to fibrosis.

What are the implications of CoQ10's potential in the context of Methotrexate treatment?

The implications are significant because CoQ10 may offer a natural defense against the adverse effects of methotrexate on the lungs and liver. If validated through further research, CoQ10 could become a valuable complementary approach for individuals undergoing methotrexate treatment. By supporting autophagy and reducing oxidative stress, CoQ10 could help to preserve lung and liver health, improving the quality of life for those using methotrexate.

What is autophagy and how does CoQ10 influence it in relation to lung and liver health?

Autophagy is a critical cellular process where cells remove damaged components to stay healthy. Methotrexate disrupts this process, which can lead to fibrosis. CoQ10 appears to reactivate autophagy, potentially reducing the severity of fibrosis. The cellular markers involved are mTOR, MAP1LC3B, p62/SQSTM1 and HMGB1. By influencing these elements, CoQ10 promotes cellular cleanup and helps maintain the health of the lungs and liver.