The pathophysiological basis of the protective effects of metformin in heart failure

Dziubak, Aleksandra; Wójcicka, Grażyna

doi:10.5604/01.3001.0010.3855

Cited by 8 publications

(3 citation statements)

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“…Metformin treatment inhibits development of adverse myocardial structural and functional changes by inhibiting the production and accumulation of AGEs[ 186 , 187 ]. Metformin also inhibits the AGE-induced VSMC proliferation[ 188 ]. Animal and in vitro models have shown the efficacy of dipeptidyl peptidase-4 inhibitors such as sitagliptin, cilizytin, vildagliptin and linalgliptin in inhibiting glycosylation, downregulating the levels of AGEs, RAGE and oxidative stress markers, and decreasing the expression of VCAM-1, PAI-1, and ICAM-1[ 189 - 192 ].…”

Section: Anti-ages Therapiesmentioning

confidence: 99%

Advanced glycation end products: Key mediator and therapeutic target of cardiovascular complications in diabetes

Bansal¹,

Burman²,

Tripathi³

2023

World J Diabetes

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The incidence of type 2 diabetes mellitus is growing in epidemic proportions and has become one of the most critical public health concerns. Cardiovascular complications associated with diabetes are the leading cause of morbidity and mortality. The cardiovascular diseases that accompany diabetes include angina, myocardial infarction, stroke, peripheral artery disease, and congestive heart failure. Among the various risk factors generated secondary to hyperglycemic situations, advanced glycation end products (AGEs) are one of the important targets for future diagnosis and prevention of diabetes. In the last decade, AGEs have drawn a lot of attention due to their involvement in diabetic patho-physiology. AGEs can be derived exogenously and endogenously through various pathways. These are a nonhomogeneous, chemically diverse group of compounds formed nonenzymatically by condensation between carbonyl groups of reducing sugars and free amino groups of protein, lipids, and nucleic acid. AGEs mediate their pathological effects at the cellular and extracellular levels by multiple pathways. At the cellular level, they activate signaling cascades via the receptor for AGEs and initiate a complex series of intracellular signaling resulting in reactive oxygen species generation, inflammation, cellular proliferation, and fibrosis that may possibly exacerbate the damaging effects on cardiac functions in diabetics. AGEs also cause covalent modifications and cross-linking of serum and extracellular matrix proteins; altering their structure, stability, and functions. Early diagnosis of diabetes may prevent its progression to complications and decrease its associated comorbidities. In the present review, we recapitulate the role of AGEs as a crucial mediator of hyperglycemia-mediated detrimental effects in diabetes-associated complications. Furthermore, this review presents an overview of future perspectives for new therapeutic interventions to ameliorate cardiovascular complications in diabetes.

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Section: Anti-ages Therapiesmentioning

confidence: 99%

Advanced glycation end products: Key mediator and therapeutic target of cardiovascular complications in diabetes

Bansal¹,

Burman²,

Tripathi³

2023

World J Diabetes

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“…[108] AGEs-induced proliferation of VSMCs was inhibited by metformin. [109,110] Thiazolidine-derived metformin reduces AGE levels in patients with polycystic ovary syndrome and reduces arteriosclerosis in young women with polycystic ovary syndrome. [111] Metformin can reduce the accumulation of AGEs and down-regulate the expression of RAGE in the kidney of diabetic rats.…”

Section: Metforminmentioning

confidence: 99%

Hypoglycemic Drugs and Advanced Glycation End products

2019

ARC Journal of Diabetes and Endocrinology

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Recent data showed that 9.1% of adults worldwide have diabetes, and 318 million adults have a high risk of developing diabetes in the future. Diabetes and its complications have serious impact on human health. In the early stages of diabetes, excessive advanced glycation endproducts (AGEs) accumulate in the body and bind to its receptor RAGE, which impairs glucose regulation. In the later stages of diabetes, increased blood glucose can accelerate the production of more AGEs. AGEs play a pivotal role in the development of diabetes and its complications. In recent years, AGEs have become one of the research hotspots. The search for potential drug targets that can block or reduce the accumulation of AGEs has attracted increasing attention. This review summarizes the role of AGEs and the effects of various hypoglycemic agents on AGEs from the perspective of mechanisms, in order to provide reference for the further search for targeted drugs against AGEs.

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“…Metformin can also inhibit the generation and accumulation of advanced gyration end products (AGEs) and thereby prevents the development of the adverse structural and functional changes in myocardium. In summary, experimental and clinical data indicate the ability of metformin to prevent the development of the structural and functional changes in myocardium, although further basic research and clinical studies assessing bene its and safety of metformin therapy in patients with HF are required" [16].…”

Section: From Literaturementioning

confidence: 99%

New pharmacological strategies in some metabolic endocrine disorder under a toxicological approach

Luisetto¹

2017

Ann Clin Endocrinol Metabol

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In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies effi cacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (effi cacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really effi cacy drugs strategy that show a profi le of effi cacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?

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The pathophysiological basis of the protective effects of metformin in heart failure

Cited by 8 publications

References 0 publications

Advanced glycation end products: Key mediator and therapeutic target of cardiovascular complications in diabetes

Advanced glycation end products: Key mediator and therapeutic target of cardiovascular complications in diabetes

Hypoglycemic Drugs and Advanced Glycation End products

New pharmacological strategies in some metabolic endocrine disorder under a toxicological approach

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