A new study by researchers from Medical College of Wisconsin Milwaukee-USA has found that cardiac fibrosis is yet another causative effect of exposure to the SARS-CoV-2 virus
The study findings were published in the peer reviewed Journal of the American Heart Association.
https://www.ahajournals.org/doi/full/10.1161/JAHA.122.027990
Fibrosis is an essential adaptive response after tissue injury. However, excess production causes organ failure, accounting for one‐third of deaths worldwide.1
Chaperones, including HSP47, maintain proteostasis in the endoplasmic reticulum and regulate the biosynthesis, folding, and secretion of procollagen. GRP78, an endoplasmic reticulum–resident chaperone and a SARS‐CoV‐2 coreceptor, is elevated in pneumocytes and alveolar macrophages (CD68+ cells) in autopsies of patients with COVID‐19.3
Because cardiac fibrosis predicts arrythmias and sudden cardiac death in adjudicated human autopsies, efforts to understand mechanisms that lead to cardiac fibrosis among COVID‐19 survivors are urgently needed.4, 5, 6
Herein, we identified COVID‐19–associated increases in 2 cardiac cell types, myofibroblasts and macrophages, which have been associated with tissue repair and fibrosis and have also been linked to enhanced fibrosis experimentally and theoretically.7
To circumvent challenges in accuracy of tissue sampling by invasive endomyocardial biopsy, we used human autopsy tissue, which uniquely enables the simultaneous assessment of clinicomorphological, molecular, and immunohistochemical events at single‐cell resolution in situ.
Discussion
Our data identify increased HSP47+ and CD163+ cells and increased collagen I deposition in hot spots within hearts after SARS‐CoV‐2 infection.
These changes may be the first evidence of a COVID‐19–related profibrotic phenotype in human hearts in situ.
As such, COVID‐19–induced cardiac fibrosis may have critical long‐term public health implications for health care systems and policy makers.12 Our work suggests investigations into mechanisms of viral‐induced integrated stress response pathways, myofibroblast lineage transitional states, and paracrine mediators are priorities.
One immediate implication is development of noninvasive approaches (ie, plasma biomarkers and noninvasive imaging) to identify antemortem profibrotic phenotypes. These data may also accelerate clinical trials of antifibrotic therapies and could influence policies addressing cardiovascular health disparities among vulnerable populations.
