SARS-CoV-2 (COVID-19) has primarily affected older patients and those with certain pre-existing conditions since its inception. Specifically, between 20% and 25% of all COVID-19-related deaths occurred in people who already had cardiovascular disease.
More concerning, a significant number of those who recovered from the virus, even those who experienced only mild symptoms, are now showing signs of long-term heart problems as a result of the infection.
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It is now a critical medical need to understand what causes and how these effects occur. Dr Zhiqiang Lin, Assistant Professor at the Masonic Medical Research Institute (MMRI), recently published two papers establishing a link between SARS-CoV-2 and heart disease.
Even prior to the pandemic, the Lin Laboratory was studying a class of pattern recognition receptor proteins known as Toll-Like Receptors (TLRs), which act as antennas for detecting invading pathogens.
They discovered that the majority of TLRs were expressed at low levels in neonatal mouse hearts but at high levels in adult mouse hearts, and that several TLRs (including TLR4, which is toxic when activated) were upregulated in response to pathological cardiac stressors such as hypertension and heart attack.
Additionally, they demonstrated that activating TLR4 activity in a subset of heart muscle cells predisposes the heart to a systemic inflammatory response.
This study, titled “YAP/TEAD1 Complex Is a Default Repressor of Cardiac Toll-Like Receptor Genes”, was published in the International Journal of Molecular Science (mdpi.com/1422-0067/22/13/6649).
SARS-CoV-2 infection in humans is dependent on ACE2, a critical enzyme that lowers blood pressure. The SARS-CoV-2 spike protein, which protrudes from the viral membrane during infection, binds to the host cell’s ACE2 and facilitates virus entry.
As a result, one of the leading hypotheses at the moment is that SARS-CoV-2 caused heart damage by impairing ACE2 function. Dr Lin’s goal, however, was to ascertain the existence of another possible pathological mechanism: that the cardiac consequences of COVID-19 infection were partially caused by TLR4 hyperactivation.
His group established that TLR4 recognized SARS-CoV-2 Spike protein, and his laboratory’s data indicated that simple overexpression of SARS-CoV-2 Spike protein in the mouse heart was sufficient to induce heart dysfunction and inflammation. Because Spike protein interacts with murine TLR4, but not with murine ACE2, Dr Lin’s data emphasizes the critical role of TLR4 signalling in the pathogenesis of COVID-19-induced cardiac injury.
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Additionally, this study elucidates why the cardiac injury may occur more frequently in COVID-19 patients with pre-existing cardiac disease.
This research paper was published in BioRxiv (biorxiv.org/content/10.1101/2021.06.20.448993v1).
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