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All Studies   Meta Analysis    Recent:   

Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism

Hou et al., Scientific Reports, doi:10.1038/s41598-024-63081-0
May 2024  
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Metformin for COVID-19
3rd treatment shown to reduce risk in July 2020
 
*, now with p < 0.00000000001 from 91 studies.
No treatment is 100% effective. Protocols combine treatments. * >10% efficacy, ≥3 studies.
4,300+ studies for 77 treatments. c19early.org
In Silico and In Vitro study showing metformin as a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism. Authors identified PTEN and mTOR as potential core target genes of metformin for treating COVID-19/LUAD. Bioinformatics analysis suggests metformin's mechanism may involve energy metabolism, NADH oxidoreductase activity, FoxO signaling, AMPK signaling, and mTOR signaling pathways. In A549 lung adenocarcinoma cells, metformin increased PTEN expression, decreased mTOR expression, inhibited cell proliferation and colony formation, increased glucose consumption and lactate production, and decreased ATP production and NAD+/NADH ratio.
12 preclinical studies support the efficacy of metformin for COVID-19:
A systematic review and meta-analysis of 15 non-COVID-19 preclinical studies showed that metformin inhibits pulmonary inflammation and oxidative stress, minimizes lung injury, and improves survival in animal models of acute respiratory distress syndrome (ARDS) or acute lung injury (ALI)10. Metformin inhibits SARS-CoV-2 in vitro7,8, minimizes LPS-induced cytokine storm in a mouse model9, minimizes lung damage and fibrosis in a mouse model of LPS-induced ARDS6, may protect against SARS-CoV-2-induced neurological disorders5, may be beneficial via inhibitory effects on ORF3a-mediated inflammasome activation11, reduces UUO and FAN-induced kidney fibrosis6, increases mitochondrial function and decreases TGF-β-induced fibrosis, apoptosis, and inflammation markers in lung epithelial cells6, may reduce inflammation, oxidative stress, and thrombosis via regulating glucose metabolism1, attenuates spike protein S1-induced inflammatory response and α-synuclein aggregation4, and may improve outcomes via modulation of immune responses with increased anti-inflammatory T lymphocyte gene expression and via enhanced gut microbiota diversity12.
Hou et al., 30 May 2024, peer-reviewed, 9 authors. Contact: 408931519@qq.com, zbzb612@126.com.
In Vitro studies are an important part of preclinical research, however results may be very different in vivo.
This PaperMetforminAll
Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism
Yongwang Hou, Zhicong Yang, Baoli Xiang, Jiangmin Liu, Lina Geng, Dandan Xu, Minghua Zhan, Yuhuan Xu, Bin Zhang
Scientific Reports, doi:10.1038/s41598-024-63081-0
Lung adenocarcinoma (LUAD) is the most common and aggressive subtype of lung cancer, and coronavirus disease 2019 (COVID-19) has become a serious public health threat worldwide. Patients with LUAD and COVID-19 have a poor prognosis. Therefore, finding medications that can be used to treat COVID-19/LUAD patients is essential. Bioinformatics analysis was used to identify 20 possible metformin target genes for the treatment of COVID-19/LUAD. PTEN and mTOR may serve as hub target genes of metformin. Metformin may be able to cure COVID-19/LUAD comorbidity through energy metabolism, oxidoreductase NADH activity, FoxO signalling pathway, AMPK signalling system, and mTOR signalling pathway, among other pathways, according to the results of bioinformatic research. Metformin has ability to inhibit the proliferation of A549 cells, according to the results of colony formation and proliferation assays. In A549 cells, metformin increased glucose uptake and lactate generation, while decreasing ATP synthesis and the NAD + /NADH ratio. In summary, PTEN and mTOR may be potential targets of metformin for the treatment of COVID-19/ LUAD. The mechanism by which metformin inhibits lung adenocarcinoma cell proliferation may be related to glucose metabolism regulated by PI3K/AKT signalling and mTOR signalling pathways. Our study provides a new theoretical basis for the treatment of COVID-19/LUAD.
Ethics approval and consent to participate This study did not require ethical board approval because it did not include human or animal trials. Author contributions Bin Zhang: Conceptualization. Baoli Xiang: Methodology, Software. Yongwang Hou: Data curation, Writing-Original draft preparation, funding acquisition. Jiangmin Liu: Visualization, Investigation. Lina Geng and Yuhuan Xu: Supervision. Dandan Xu and Minghua Zhan: Software, Validation. Zhicong Yang: Writing-Reviewing and Editing. All authors have reviewed the results and approved the final version of the manuscript. Competing interests The authors declare no competing interests. Additional information Supplementary Information The online version contains supplementary material available at https:// doi. org/ 10. 1038/ s41598-024-63081-0. Correspondence and requests for materials should be addressed to Y.H. or B.Z. Reprints and permissions information is available at www.nature.com/reprints. Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Caloric restriction and metformin selectively improved ' 'LKB1-mutated NSCLC tumor response to chemo- and chemo-immunotherapy. J. ' 'Exp. Clin. Cancer Res. 43, 6 (2024).', 'journal-title': 'J. Exp. Clin. Cancer Res.'}, { 'key': '63081_CR31', 'doi-asserted-by': 'publisher', 'first-page': '6', 'DOI': '10.1186/s13046-019-1503-6', 'volume': '39', 'author': 'D Jin', 'year': '2020', 'unstructured': 'Jin, D. et al. Metformin-repressed miR-381-YAP-snail axis activity ' 'disrupts NSCLC growth and metastasis. J. Exp. Clin. Cancer Res. 39, 6 ' '(2020).', 'journal-title': 'J. Exp. Clin. Cancer Res.'}, { 'key': '63081_CR32', 'doi-asserted-by': 'publisher', 'first-page': '253', 'DOI': '10.1016/j.lfs.2018.07.046', 'volume': '208', 'author': 'W Qian', 'year': '2018', 'unstructured': 'Qian, W. et al. Metformin suppresses tumor angiogenesis and enhances the ' 'chemosensitivity of gemcitabine in a genetically engineered mouse model ' 'of pancreatic cancer. 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Rep.'}, { 'key': '63081_CR38', 'doi-asserted-by': 'publisher', 'first-page': '967', 'DOI': '10.1016/j.tcb.2023.03.008', 'volume': '33', 'author': 'J Liu', 'year': '2023', 'unstructured': 'Liu, J. & Cao, X. Glucose metabolism of TAMs in tumor chemoresistance ' 'and metastasis. Trends Cell Biol. 33, 967–978 (2023).', 'journal-title': 'Trends Cell Biol.'}, { 'key': '63081_CR39', 'doi-asserted-by': 'publisher', 'first-page': '158', 'DOI': '10.1186/s12935-024-03314-4', 'volume': '24', 'author': 'Y Hu', 'year': '2024', 'unstructured': 'Hu, Y. et al. Flavokawain C inhibits glucose metabolism and tumor ' 'angiogenesis in nasopharyngeal carcinoma by targeting the ' 'HSP90B1/STAT3/HK2 signaling axis. Cancer Cell Int. 24, 158 (2024).', 'journal-title': 'Cancer Cell Int.'}, { 'key': '63081_CR40', 'doi-asserted-by': 'publisher', 'first-page': '283', 'DOI': '10.1016/j.it.2022.02.001', 'volume': '43', 'author': 'M Zheng', 'year': '2022', 'unstructured': 'Zheng, M., Schultz, M. B. & Sinclair, D. A. NAD(+) in COVID-19 and viral ' 'infections. Trends Immunol. 43, 283–295 (2022).', 'journal-title': 'Trends Immunol.'}, { 'key': '63081_CR41', 'doi-asserted-by': 'publisher', 'first-page': '2052', 'DOI': '10.1056/NEJMra1704560', 'volume': '379', 'author': 'MD Goncalves', 'year': '2018', 'unstructured': 'Goncalves, M. D., Hopkins, B. D. & Cantley, L. C. Phosphatidylinositol ' '3-kinase, growth disorders, and cancer. N. Engl. J. Med. 379, 2052–2062 ' '(2018).', 'journal-title': 'N. Engl. J. Med.'}, { 'key': '63081_CR42', 'doi-asserted-by': 'publisher', 'first-page': '2419', 'DOI': '10.7150/jca.63152', 'volume': '13', 'author': 'S Wang', 'year': '2022', 'unstructured': 'Wang, S., Zhang, H., Du, B., Li, X. & Li, Y. Fuzzy planar cell polarity ' 'gene (FUZ) promtes cell glycolysis, migration, and invasion in non-small ' 'cell lung cancer via the phosphoinositide 3-kinase/protein kinase B ' 'pathway. J. Cancer 13, 2419–2429 (2022).', 'journal-title': 'J. Cancer'}, { 'key': '63081_CR43', 'doi-asserted-by': 'publisher', 'first-page': '808', 'DOI': '10.3390/biom11060808', 'volume': '11', 'author': 'S Deinhardt-Emmer', 'year': '2021', 'unstructured': 'Deinhardt-Emmer, S. et al. Inhibition of phosphatidylinositol 3-kinase ' 'by pictilisib blocks influenza virus propagation in cells and in lungs ' 'of infected mice. Biomolecules 11, 808 (2021).', 'journal-title': 'Biomolecules'}, { 'key': '63081_CR44', 'doi-asserted-by': 'publisher', 'first-page': '2165', 'DOI': '10.1007/s00705-020-04740-1', 'volume': '165', 'author': 'J Blanco', 'year': '2020', 'unstructured': 'Blanco, J., Cameirao, C., Lopez, M. C. & Munoz-Barroso, I. ' 'Phosphatidylinositol-3-kinase-Akt pathway in negative-stranded RNA virus ' 'infection: A minireview. Arch. Virol. 165, 2165–2176 (2020).', 'journal-title': 'Arch. Virol.'}, { 'key': '63081_CR45', 'doi-asserted-by': 'publisher', 'first-page': '422', 'DOI': '10.1128/JVI.01671-10', 'volume': '85', 'author': 'EF Dunn', 'year': '2011', 'unstructured': 'Dunn, E. F. & Connor, J. H. Dominant inhibition of Akt/protein kinase B ' 'signaling by the matrix protein of a negative-strand RNA virus. J. ' 'Virol. 85, 422–431 (2011).', 'journal-title': 'J. Virol.'}, { 'key': '63081_CR46', 'doi-asserted-by': 'publisher', 'DOI': '10.1111/cpr.13304', 'volume': '55', 'author': 'L Che', 'year': '2022', 'unstructured': 'Che, L. et al. Intracellular antibody targeting HBx suppresses invasion ' 'and metastasis in hepatitis B virus-related hepatocarcinogenesis via ' 'protein phosphatase 2A–B56gamma-mediated dephosphorylation of protein ' 'kinase B. Cell Prolif. 55, e13304 (2022).', 'journal-title': 'Cell Prolif.'}, { 'key': '63081_CR47', 'first-page': '2939', 'volume': '15', 'author': 'Y He', 'year': '2018', 'unstructured': 'He, Y. et al. 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