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It didn’t take long into our indoctrination with COVID-19 to learn it was more than just a respiratory virus capable of doing lung damage.
Looking back, researchers have been able to see the dangers the virus holds for the heart, which can lead to long-term damage and even death.
Now, researchers may have finally discovered why in a study that has proven that COVID strikes at the very power source of cells responsible for helping the heart keep ticking — the mitochondria.
Mitochondrial gene expression and COVID-19
Past research demonstrated the ability of proteins of the SARS-CoV-2 virus to bind to mitochondrial proteins in host cells, leading to mitochondrial dysfunction.
However, it was unclear just how much the mitochondria that power various organs in the body are affected and how long the problems last.
So a team of researchers at the Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT) set out to find the answers.
To do so, they analyzed mitochondrial gene expression in both nasopharyngeal and autopsy tissues from patients infected with COVID-19, as well as animal models.
“The tissue samples from human patients allowed us to look at how mitochondrial gene expression was affected at the onset and end of disease progression,” said the study’s first author Joseph Guarnieri, PhD. “… while animal models allowed us to fill in the blanks and look at the progression of gene expression differences over time.”
Long-term organ damage
What they found is that while the lungs initially suffer from the infection, they eventually begin to recover.
That is happy news that unfortunately does not extend to the heart or other organs, like the liver and kidneys.
The team found that when the viral load was at its peak in the lungs, mitochondrial gene expression was diminished in the brain – specifically in the cerebellum. This was even though the virus was undetectable in the brain itself.
However, that mitochondrial function began to recover midway through the infection.
On the other hand, mitochondrial function in the other organs, particularly the heart, remained impaired even after “recovery” from the infection.
“This study provides us with strong evidence that we need to stop looking at COVID-19 as strictly an upper respiratory disease and start viewing it as a systemic disorder that impacts multiple organs,” said co-senior author, Douglas Wallace, PhD. “The continued dysfunction we observed in organs other than the lungs suggests that mitochondrial dysfunction could be causing long-term damage to the internal organs of these patients.”
Mitochondrial damage and long COVID
In 2022, researchers found that people living with long COVID symptoms have mitochondria that no longer function properly — and that impacts not only dysfunction in muscle tissues but also in pulmonary and neurological systems as well.
Researchers plan to build upon all of these discoveries to understand better how the virus alters cells and how those effects can be reversed or repaired.
PQQ is considered a longevity vitamin because mitochondria decrease and become dysfunctional with age. Some studies have reported that PQQ can raise mitochondrial activity in both animal and human studies.
Good sources of CoQ10 are fatty fish, broccoli, peanuts and pistachios. Be mindful that some statins decrease CoQ10. Some foods containing PQQ include fermented soybeans, tofu, celery, green pepper, kiwi, fava beans and orange foods like carrots, papaya, sweet potato and oranges.
Editor’s note: There are numerous safe and natural ways to decrease your risk of blood clots including the 25-cent vitamin, the nutrient that acts as a natural blood thinner and the powerful herb that helps clear plaque. To discover these and more, click here for Hushed Up Natural Heart Cures and Common Misconceptions of Popular Heart Treatments!
Study Finds COVID-19 Causes Mitochondrial Dysfunction in Heart and Other Organs – Integrative Practitioner