Jack Hadfield: SARS-CoV-2–Associated Lasting Mitochondrial Injury in Cardiomyocytes
Jack Hadfield, Co-founder and Research Lead at Amatica Health, shared a post on Linkedin:
“Study shows SARS-CoV-2 can cause direct damage to heart cell mitochondria, even weeks to months after infection, potentially helping explain long COVID heart symptoms like chest pain, palpitations, and fatigue.
Let’s break it down.
Researchers studied 5 people who had previously had COVID-19 and later developed new or unusual heart problems, including chest pain, irregular heartbeat, and even cardiac arrest.
Each patient underwent a heart biopsy, meaning a small sample of heart tissue was examined under a microscope.
All 5 were diagnosed with myocarditis, which is inflammation and injury in the heart muscle. But this was not classic myocarditis with large immune cell infiltration.
Inflammation was relatively mild. The striking finding was structural damage inside the heart muscle cells themselves.
Using electron microscopy, the researchers found that mitochondria, the energy-producing parts of cells, were swollen, full of holes, and had lost their cristae, the inner folds needed to generate energy efficiently. Around 40 to 60% of mitochondria were damaged in each patient.
This was still seen 2 to 3 months after COVID-19 in some patients, suggesting the damage can persist well beyond the acute infection.
Since mitochondria produce ATP, the main energy currency of the cell, this kind of injury could plausibly contribute to fatigue and ongoing heart symptoms.
They also found fibrosis, signs of cell aging, and damage to myofibrils, which are the structures needed for heart muscle contraction. Together, this points to meaningful heart cell injury even when standard imaging may not show obvious abnormalities.
One case was a healthy 30-year-old man who collapsed during exercise from cardiac arrest 5 weeks after COVID-19. He had no blocked arteries and no prior heart disease. Biopsy showed severe mitochondrial damage and mild myocarditis.
Another patient had chest pain despite normal CMR, echo, and ECG results. The biopsy was what revealed the underlying mitochondrial and cellular injury.
To test whether SARS-CoV-2 could drive this directly, the researchers infected mice with Omicron variants.
Just 7 days later, mouse heart cells showed the same mitochondrial abnormalities, including swelling, vacuoles, and cristae loss. Around 60 to 75% of mitochondria were damaged in infected mice, while controls showed none of this.
Proteomic analysis also found major disruption in mitochondrial pathways, including protein import systems, energy production machinery, and antioxidant defenses.
Even though some pathways appeared upregulated, likely as a compensatory response, the core structural damage remained.
Importantly, no viral proteins were found in the mouse hearts at day 7, suggesting this injury may persist even after the virus itself is no longer present in the tissue.
Bottom line: SARS-CoV-2 appears capable of causing lasting mitochondrial injury in heart muscle cells.”
Proceed to the video attached to the post.
Title:SARS-CoV-2 damages cardiomyocyte mitochondria and implicates long COVID-associated cardiovascular manifestations
Authors: Wenliang Che, Shuai Guo, Yanqun Wang, Xiaohua Wan, Bingyu Tan, Hailing Li, Jiasuer Alifu, Mengyun Zhu, Zesong Chen, Peiyao Li, Lei Zhang, Zhaoyong Zhang, Yiliang Wang, Xiaohan Huang, Xinsheng Wang, Jian Zhu, Xijiang Pan, Fa Zhang, Peiyi Wang, Sen-Fang Sui, Jincun Zhao, Yawei Xu, Zheng Liu
Read the Full Article on Journal of Advanced Research
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