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MicroRNA-155 mediates endogenous angiotensin ii type 1 receptor regulation:implications for innovative type 2 diabetes mellitus management

引用

世界糖尿病杂志:英文版(电子版) 2023年第9期14卷 1334-1340页

作者： Konstantinos I Papadopoulos Alexandra Papadopoulou Tar-Choon Aw Department of R&D THAI StemLifeBangkok 10310Thailand Occupational and Environmental Health Services Feelgood LundLund 223-63SkåneSweden Department of Laboratory Medicine Changi General HospitalSingapore 529889SingaporeSingapore Department of Medicine National University of SingaporeSingapore 119228SingaporeSingapore

type 2 diabetes mellitus(T2DM)is a lifelong condition and a threat to human health.Thorough understanding of its pathogenesis is acutely needed in order to devise innovative,preventative,and potentially curative pharmacological interventions.MicroRNAs(miRNA),are small,non-coding,one-stranded RNA molecules,that can target and silence around 60%of all human genes through translational repression.MiR-155 is an ancient,evolutionarily well-conserved miRNA,with distinct expression profiles and multifunctionality,and a target repertoire of over 241 genes involved in numerous physiological and pathological processes including hematopoietic lineage differentiation,immunity,inflammation,viral infections,cancer,cardiovascular conditions,and particularly diabetes mellitus.MiR-155 Levels are progressively reduced in aging,obesity,sarcopenia,and T2DM.Thus,the loss of coordinated repression of multiple miR-155 targets acting as negative regulators,such as C/EBPβ,HDAC4,and SOCS1 impacts insulin signaling,deteriorating glucose homeostasis,and causing insulin resistance(IR).Moreover,deranged regulation of the renin angiotensin aldosterone system(RAAS)through loss of angiotensin ii type 1 receptor downregulation,and negated repression of ETS-1,results in unopposed detrimental angiotensin ii effects,further promoting IR.Finally,loss of BACH1 and SOCS1 repression abolishes cytoprotective,anti-oxidant,anti-apoptotic,and anti-inflam matory cellular pathways,and promotesβ-cell loss.In contrast to RAAS inhibitor treatments that further decrease already reduced miR-155 Levels,strategies to increase an ailing miR-155 production in T2DM,e.g.,the use of metformin,mineralocorticoid receptor blockers(spironolactone,eplerenone,finerenone),and verapamil,alone or in various combinations,represent current treatment options.In the future,direct tissue delivery of miRNA analogs is likely.

关键词： angiotensin ii angiotensin ii type 1 receptor Arginase 2 L-type calcium channel Mineralocorticoid receptor MiRNA-155 Renin-angiotensin aldosterone system type 1/2 diabetes mellitus Verapamil

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