ArticleJournal of cellular and molecular medicine2020
STAT3 isoforms differentially affect ACE2 expression: A potential target for COVID-19 therapy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Daphnetin may protect from SARS-CoV-2 infection by reducing ACE2.Scientific reports · 2024Article
- Proteomic snapshot of saliva samples predicts new pathways implicated in SARS-CoV-2 pathogenesis.Clinical proteomics · 2024Article
- Systems pharmacology dissection of pharmacological mechanisms of Xiaochaihu decoction against human coronavirus.BMC complementary medicine and therapies · 2023Article
- Article
- CDK4/6 inhibitor palbociclib promotes SARS-CoV-2 cell entry by down-regulating SKP2 dependent ACE2 degradation.Antiviral research · 2023Article
- Transcriptional regulation and small compound targeting of ACE2 in lung epithelial cells.Acta pharmacologica Sinica · 2022Article
- Article
- Contribution of STAT3 to the pathogenesis of COVID-19.Microbial pathogenesis · 2021Review
- Network-Based Identification and Experimental Validation of Drug Candidates Toward SARS-CoV-2Frontiers in genetics · 2021Article
- SARS-CoV-2-induced Overexpression of miR-4485 Suppresses Osteogenic Differentiation and Impairs Fracture Healing.International journal of biological sciences · 2021Article
- STAT3 isoforms differentially affect ACE2 expression: A potential target for COVID-19 therapy.Journal of cellular and molecular medicine · 2020Article
- Potential Simultaneous Inhibitors of Angiotensin-Converting Enzyme 2 and Transmembrane Protease, Serine 2.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SARS-coronavirus 2 is the aetiologic agent COVID-19. ACE2 has been identified as a cell entry receptor for the virus. Therefore, trying to understand how the gene is controlled has become a major goal. We silenced the expression of STAT3α and STAT3β, and found that while silencing STAT3α causes an increase in ACE2 expression, silencing STAT3β causes the opposite effect. Studying the role of STAT3 in ACE2 expression will shed light on the molecular events that contribute to the progression of the disease and that the different roles of STAT3α and STAT3β in that context must be taken in consideration. Our results place STAT3 in line with additional potential therapeutic targets for treating COVID-19 patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.