
IndraLab
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"Metformin, the most widely used drug for treating T2D, can inhibit NLRP3 by activating AMPK (AMP activated protein kinase), thus increasing autophagy activity to promote the clearance of inflammasomes via inhibiting the mTOR pathway and alleviating the symptoms in diabetic cardiomyopathy."
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"Among the last ones, a remarkable effect of metformin in preventing LPS-induced IL-1β mRNA levels was found, thus further supporting our in vitro study showing that metformin highly inhibits NLRP3 inflammasome priming in microglia.Under brain pathological conditions, microglial checkpoints pathways sense the environment to prevent overreaction to external stimuli."
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"In addition, metformin, a drug widely used for diabetes, was reported to indirectly inhibit the NLRP3 inflammasome via the regulation of the mechanistic target of rapamycin mechanistic target of rapamycin kinase (mTOR) protein, which is related to the reduction in the mortality of COVID-19 and type 2 diabetes mellitus (T2DM) patients [149]."
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"Although metformin attenuated mtROS accumulation in macrophages treated with the NLRP3 activators ATP and nigericin, this effect was not important for inhibition of NLRP3 inflammasome activation which was not reversed by treatment of metformin incubated macrophages with the mtROS generators mitoParaquat and DMNQ."
| PMC
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"[55] Besides, metformin a first-line drug in the management of T2DM, acts through activation of AMP-activated protein kinase (AMPK) and blocking of mitochondrial complex I. [56] Metformin inhibits NLRP3 inflammasome through AMPK activation and autophagy with mTOR pathway inhibition in dilated cardiomyopathy."
| DOI
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"[55]
Besides, metformin a first-line drug in the management of T2DM, acts through activation of AMP-activated protein kinase (AMPK) and blocking of mitochondrial complex I. [56] Metformin inhibits NLRP3 inflammasome through AMPK activation and autophagy with mTOR pathway inhibition in dilated cardiomyopathy."