Metformin in SLE: metabolism as a therapeutic target in autoimmune disease. Nikpour, M. The Lancet Rheumatology, 2(4):e196–e197, April, 2020. Publisher: Elsevier
Metformin in SLE: metabolism as a therapeutic target in autoimmune disease [link]Paper  doi  abstract   bibtex   
The central role of metabolism in the modulation of immune responses is increasingly recognised in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE).1 Accordingly, it is not implausible that metformin, an anti-diabetic drug that regulates systemic and cellular metabolism, might have a disease-modifying effect in SLE. Indeed, metformin has been shown to have metabolic effects in many lineages of immune cell, including T-helper and regulatory T cells, neutrophils, and dendritic cells, which are all key mediators of the autoimmunity and inflammation that are characteristic of SLE.
@article{nikpour_metformin_2020,
	title = {Metformin in {SLE}: metabolism as a therapeutic target in autoimmune disease},
	volume = {2},
	issn = {2665-9913},
	shorttitle = {Metformin in {SLE}},
	url = {https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30040-0/abstract},
	doi = {10.1016/S2665-9913(20)30040-0},
	abstract = {The central role of metabolism in the modulation of immune responses is increasingly
recognised in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus
(SLE).1 Accordingly, it is not implausible that metformin, an anti-diabetic drug that
regulates systemic and cellular metabolism, might have a disease-modifying effect
in SLE. Indeed, metformin has been shown to have metabolic effects in many lineages
of immune cell, including T-helper and regulatory T cells, neutrophils, and dendritic
cells, which are all key mediators of the autoimmunity and inflammation that are characteristic
of SLE.},
	language = {English},
	number = {4},
	urldate = {2020-05-22},
	journal = {The Lancet Rheumatology},
	author = {Nikpour, Mandana},
	month = apr,
	year = {2020},
	note = {Publisher: Elsevier},
	pages = {e196--e197},
}

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