ArticleAmerican journal of physiology. Cell physiology2025
Decoding fibrosis in nonresolvable COVID-19: a role for myeloid-specific HIF1A deletion.
Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
A complication of viral lung infections is the development of pulmonary fibrosis. This phenomenon is most evident in patients with COVID-19, where in its most aggressive form patients developed nonresolvable (NR) COVID-19 requiring lung transplantation. NR-COVID-19 was characterized by the presentation of a fulminant fibrotic lung injury that progressed rapidly, even in patients with limited comorbidities. However, the mechanisms that led to this rapidly progressing form of fibrosis are not fully understood. A common clinical manifestation in the most severe cases of COVID-19 was the presence of "silent" hypoxemia. Thus, we hypothesized that a dysfunctional hypoxic response may result in exacerbated lung injury seen in patients with severe forms of COVID-19. Our results demonstrate that despite increased expression of hypoxia-inducible factor 1A (HIF1A) and its downstream mediator adenosine A
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