At the time of writing, the SARS-CoV-2 virus, responsible for COVID-19, has infected more than 28 million people worldwide, with nearly a million deaths attributed to the virus (source: Johns Hopkins Coronavirus Resource Center). One of the most striking aspects of SARS-CoV-2 infection is the diversity of symptoms that have been reported in patients.1
View the full Mechanisms of Fibrosis interactive pathway on the CST website.
SARS-CoV-2 was first identified, and remains primarily described, as a respiratory virus, eliciting an “Acute Respiratory Distress Syndrome” (ARDS), in similar fashion to the SARS and MERS coronavirus outbreaks in 2003 and 2010, respectively. It has become apparent however, as the SARS-CoV-2 virus has spread incessantly throughout the globe, that the effects of infection can extend well beyond an acute respiratory infection.2 Potentially serious symptoms attributed to COVID-19 include: cardiovascular complications, including hypertension, blood clots, strokes and embolisms3; heart damage (e.g., myocarditis), attributed primarily to inflammation of the heart muscle4; and neurological damage, eliciting effects ranging from a diminished sense of taste and/or smell to more severe neurological events such as dizziness, confusion, and even coma.5
Due to its relatively recent emergence in the human population, it remains difficult for scientists to predict the long-term health effects of COVID-19, particularly considering its diversity of effects during acute infection. The most severe impacts appear to manifest in tissues with high levels of vascularization (e.g., lungs, heart, kidney, liver), and it is evident that the virus elicits a significant inflammatory response in infected tissues.6 What scientists do know is that the wound healing response elicited during severe inflammation can lead to permanent tissue and organ damage, through a process of scarring called fibrosis. Similar to what was reported for both SARS and MERS, there is now evidence emerging from patients infected with SARS-CoV-2 that fibrotic damage to infected tissues can lead to health complications that persist well beyond the period of viral infection.6
Fibrosis is fundamentally a pathological wound healing response that results in significant architectural remodeling of the extracellular environment. A primary outcome of fibrosis is reduced tissue elasticity, leading to organ dysfunction where elasticity is required for normal function (e.g., lungs, heart). Key biomarkers of fibrotic onset include myofibroblast activation (α-smooth muscle actin) and increased deposition of extracellular matrix (ECM) proteins such as collagens (e.g., COL1A1, COL3A1, COL11A1), fibronectins (e.g., FN-1), and various associated matrix molecules (LOX, MMPs, hydroxyproline). Fibrosis is also associated the activation of pro-inflammatory signaling pathways, including TNF-α, interferons and interleukins, key drivers of the wound healing response.
CST has built a robust portfolio of antibody reagents to enable to research into fibrotic diseases and inflammation—the TGF-β Fibrosis Pathway Antibody Sampler Kit #77397 is a great place to start. These reagents are designed to help researchers understand the etiology of fibrotic diseases, leading to better treatments to minimize its impact.
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