Metformin and insulin-resistant related diseases: Emphasis on the role of microRNAs

被引:27
作者
Alimoradi, Nahid [1 ]
Firouzabadi, Negar [1 ]
Fatehi, Reihaneh [1 ]
机构
[1] Shiraz Univ Med Sci, Sch Pharm, Dept Pharmacol Toxicol, Shiraz, Iran
关键词
Metformin; MicroRNAs; Insulin resistance; AMPK; Biomarker; Mechanism of action; ACTIVATED PROTEIN-KINASE; ORGANIC CATION TRANSPORTERS; INDUCED CELL-DEATH; DOWN-REGULATION; IN-VITRO; MOLECULAR-MECHANISMS; TAU-PHOSPHORYLATION; CARDIAC-HYPERTROPHY; LIPID-ACCUMULATION; SIGNALING PATHWAY;
D O I
10.1016/j.biopha.2021.111662
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Metformin is one of the most prescribed drugs in type II diabetes (T2DM) which has recently found new applications in the prevention and treatment of various illnesses, from metabolic disorders to cardiovascular and age-related diseases. Metformin improves insulin resistance (IR) by modulating metabolic mechanisms and mitochondrial biogenesis. Alternation of microRNAs (miRs) in the treatment of IR-related illnesses has been observed by metformin therapy. MiRs are small non-coding RNAs that play important roles in RNA silencing, targeting the 3'untranslated region (3'UTR) of most mRNAs and inhibiting the translation of related proteins. As a result, their dysregulation is associated with many diseases. Metformin may alter miRs levels in the treatment of various diseases by AMPK-dependent or AMPK-independent mechanisms. Here, we summarized the therapeutic role of metformin by modifying the aberrant expression of miRs as potential biomarkers or therapeutic targets in diseases in which IR plays a key role.
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页数:12
相关论文
共 215 条
[1]   MiR-26b, Upregulated in Alzheimer's Disease, Activates Cell Cycle Entry, Tau-Phosphorylation, and Apoptosis in Postmitotic Neurons [J].
Absalon, Sabrina ;
Kochanek, Dawn M. ;
Raghavan, Venkatesan ;
Krichevsky, Anna M. .
JOURNAL OF NEUROSCIENCE, 2013, 33 (37) :14645-14659
[2]   Anti-Angiogenic miR-222, miR-195, and miR-21a Plasma Levels in T1DM Are Improved by Metformin Therapy, Thus Elucidating Its Cardioprotective Effect: The MERIT Study [J].
Ahmed, Fahad W. ;
Bakhashab, Sherin ;
Bastaman, Inda T. ;
Crossland, Rachel E. ;
Glanville, Michael ;
Weaver, Jolanta U. .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2018, 19 (10)
[3]   Silent information regulator 2α, a longevity factor and class III histone deacetylase, is an essential endogenous apoptosis inhibitor in cardiac myocytes [J].
Alcendor, RR ;
Kirshenbaum, LA ;
Imai, S ;
Vatner, SF ;
Sadoshima, J .
CIRCULATION RESEARCH, 2004, 95 (10) :971-980
[4]   Metformin inhibits intracellular lipid accumulation in the murine pre-adipocyte cell line, 3T3-L1 [J].
Alexandre, K. B. ;
Smit, A. M. ;
Gray, I. P. ;
Crowther, N. J. .
DIABETES OBESITY & METABOLISM, 2008, 10 (08) :688-690
[5]   Risk of pre-eclampsia in women taking metformin: a systematic review and meta-analysis [J].
Alqudah, A. ;
McKinley, M. C. ;
McNally, R. ;
Graham, U. ;
Watson, C. J. ;
Lyons, T. J. ;
McClements, L. .
DIABETIC MEDICINE, 2018, 35 (02) :160-172
[6]   Metformin attenuates cardiovascular and renal injury in uninephrectomized rats on DOCA-salt: Involvement of AMPK and miRNAs in cardioprotection [J].
Amara, Venkateswara Rao ;
Surapaneni, Sunil Kumar ;
Tikoo, Kulbhushan .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 2019, 362 :95-104
[7]   The Retinoblastoma Protein Is Essential for Survival of Postmitotic Neurons [J].
Andrusiak, Matthew G. ;
Vandenbosch, Renaud ;
Park, David S. ;
Slack, Ruth S. .
JOURNAL OF NEUROSCIENCE, 2012, 32 (42) :14809-14814
[8]  
[Anonymous], AM J TRANSL RES
[9]   Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia [J].
Ashabi, Ghorbangol ;
Khalaj, Leila ;
Khodagholi, Fariba ;
Goudarzvand, Mahdi ;
Sarkaki, Alireza .
METABOLIC BRAIN DISEASE, 2015, 30 (03) :747-754
[10]   Oxidative stress and expression of insulin signaling proteins in the brain of diabetic rats: Role of Nigella sativa oil and antidiabetic drugs [J].
Balbaa, Mahmoud ;
Abdulmalek, Shaymaa A. ;
Khalil, Sofia .
PLOS ONE, 2017, 12 (05)