Editorial: A changing panorama of diabetes outcomes: novel complications and novelties in classic complications.

The rapidly increasing prevalence of diabetes worldwide is undoubtedly one of the most serious health concerns. A significant increase in chronic complications is predicted, severely impacting the overall burden of metabolic disorders with deterioration in quality of life, increased demand for health care services, and increased health-related economics. It costs money.

Complications such as cardiovascular disease, nephropathy, retinopathy, and diabetic neuropathy are the “classic” diabetes-related long-term complications and are the most studied. The endothelium appears to be a common substrate affected by hyperglycemia, insulin resistance, and other cardiovascular risk factors. The discovery of new disease pathways in this regard has contributed to the identification of potential therapeutic targets and is expected to provide thrilling opportunities to address the vascular complications of diabetes (1). Aggressive treatment of classic cardiometabolic risk factors (2) has been linked to a reduction in cardiovascular mortality (3). However, the increased cardiovascular risk, especially posed by diabetes, remains, leading to higher mortality rates in this group (4). Furthermore, new clinical implications of classic vascular complications are being recognized. In particular, atherothrombosis has always been considered a major cardiovascular complication of diabetes;5), both epidemiological and clinical data showed that patients with diabetes have a higher incidence of heart failure and worse outcomes. In fact, the pathways leading to cardiovascular disease in patients with diabetes extend far beyond atherosclerotic coronary artery disease and include microvascular dysfunction, which can ultimately lead to impaired muscle cell contraction and relaxation. It is now well established. In fact, heart failure is the main cause of cardiovascular disease in diabetic patients, and novel research is needed to elucidate the mechanisms underlying the bidirectional association between heart failure and diabetes to improve cardiovascular disease outcomes in diabetic patients. claims (6).

Furthermore, the systemic effects of diabetes are widespread, and new complications of diabetes have recently been recognized as strong epidemiological associations have been found between diabetes and other high-morbidity diseases such as osteoporosis and neurological diseases. There is (7, 8). Undoubtedly, increases in both the prevalence of diabetes and life expectancy have led to an overall increase in the number of years people live with diabetes, a chronic and debilitating condition. This has led to an aging of the world's diabetic population and an increase in the prevalence of age-related diseases. However, there is uncertainty about the relationship between aging and diabetes, and diabetes clearly accelerates the aging of organs and tissues and the onset and progression of age-related disorders.

In this regard, the association between diabetes, vascular dysfunction, and dementia is of increasing importance, as highlighted in several articles in this special issue.

In fact, this research topic broadly discusses various new complications and novelties in classic complications. Berlanga Acosta et al. In a recent review article, we discussed the role of insulin resistance and impaired brain glucose metabolism in Alzheimer's disease (AD) and other neurodegenerative processes. AD is primarily described as a metabolic disorder, in which amyloid accumulation can appear as a byproduct of more proximal events, especially in a late-onset form. A bridge between AD and type 2 diabetes, activation of the c-Jun N-terminal kinase (JNK) pathway and subsequent serine phosphorylation of insulin response substrate (IRS)-1/2 contributes to insulin resistance and subsequent insulin resistance. You may be at a crossroads. The effects of metabolic abnormalities, as discussed in the manuscript.

Pan et al. Instead, three new classes of antidiabetic drugs have recently been announced: dipeptidyl peptidase-4 inhibitors (DPP-4is), glucagon-like peptide 1 receptor agonists (GLP-1RA), and sodium-glucose cotransporters). reviewed cardiovascular outcome trials (CVOT). -2 inhibitors (SGLT-2is) or dual inhibitors of SGLT-2 and SGLT-1 for their effects on heart failure.

Among the classic microvascular complications of diabetes, diabetic retinopathy (DR) is a significant cause of visual loss and is a subject of research where new damage mechanisms and potential treatment options are constantly being explored. Rao et al. In order to elucidate the synergistic, additive, and common damage pathways in diabetic retinopathy and to clarify the pathogenesis behind each proposed mechanism, we have investigated the effects of damage secondary to abnormalities in triglyceride and cholesterol metabolism. It depicts the mechanisms and mechanisms that are secondary to diabetes. Continue this, Augustin et al. We explain that lipids can undergo modification as a result of interaction with reactive oxygen species (ROS), supporting a role for lipid peroxidation and ALE formation in the onset and progression of this condition. Potential therapeutic approaches to prevent lipid peroxidation and lipid oxidative reactions in the diabetic retina have also been investigated, including the use of antioxidants, lipid aldehyde scavengers, and drugs to promote endogenous aldehyde detoxification systems. Includes pharmacological and gene therapy approaches. Abdelrahim et al. summarizes the available scientific evidence on the occurrence of hypoglycemic events (HE) in T2DM patients during the holy month of Ramadan and the influence of various modulating agents on the incidence of HE. Hypoglycemia is an acute complication of diabetes management and increases the risk of cardiovascular disease.

This research topic contains original research papers by the following authors: Liu et al. How pathological hyperglycemia and hyperinsulinemia seen in the prediabetic stage regulate microRNA-21 (miR-21) expression, affect downstream insulin signaling pathways, and implicate endothelial cell function. They investigated whether it could cause kidney failure or early kidney damage.

Finally, Kera. Highlighting the role of histone deacetylases in the pathogenesis of diabetic cardiomyopathy, Janapreddy et al.. We provide insights into the role of aldose reductase (AR) in the causes and consequences of diabetic cardiovascular disease and the status of AR inhibitors in clinical trials to explore potential preventive and therapeutic strategies.

The editorial article was written and reviewed by EM and KS, who co-edited the research topic. A changing panorama of diabetes outcomes: novel complications and novelties in classic complications.. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of the authors' affiliated organizations or of the publisher, editors, or reviewers. The products reviewed in this article or any claims made by their manufacturers are not endorsed or approved by the publisher.

All authors and editorial teams who contributed to the research topic A changing panorama of diabetes outcomes: novel complications and novelties in classic complications.

1. Park K, Mima A, Li Q, Rask-Madsen C, He P, Mizutani K, et al. Insulin reduces atherosclerosis by inducing endothelin receptor B expression. JCI Insights (2016) 1(6):e86574. doi: 10.1172/jci.insight.86574

PubMed abstract | CrossRef Full text | Google Scholar

2. Maddaloni E, Pozzilli P. SMART Diabetes: The Way to Go: A safe, multicomponent approach to reducing the risks of diabetes treatment. endocrine (2014) 46:3–5. doi: 10.1007/s12020-013-0128-3

PubMed abstract | CrossRef Full text | Google Scholar

3. Harding JL, Pavkoff ME, Mariano DJ, Shaw JE, Greg EW. Global trends in diabetes complications: a review of current evidence. diabetes (2019) 62:3–16. doi: 10.1007/s00125-018-4711-2

PubMed abstract | CrossRef Full text | Google Scholar

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PubMed abstract | CrossRef Full text | Google Scholar

5. Patti G, Cavallari I, Andreotti F, Calabro P, Cirillo P, Denas G, et al. Prevention of atherothrombotic events in diabetic patients: from antithrombotic therapy to new generations of hypoglycemic agents. Nat Rev Cardiol (2018) 16(2):113–30. doi: 10.1038/s41569-018-0080-2

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6. Cavallari I, Maddaloni E, Pielarice S, Muhle MT, Buzzetti R, Russian GP, ​​et al. The vicious cycle of left ventricular dysfunction and diabetes: From pathophysiology to new treatments. J Clin Endocrine Meta Tab (2020) 105:e3075–89. doi: 10.1210/clinem/dgaa427

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7. Pantaki Z, Miller ME, Rauner LJ, Williamson JD, Lazar RM, Kukiaman-Yaffee T, et al. Cognitive decline and risk of severe hypoglycemia in type 2 diabetes: post hoc Epidemiological analysis of the ACCORD trial. diabetes care (2012) 35:787–93. doi: 10.2337/dc11-1855

PubMed abstract | CrossRef Full text | Google Scholar

8. Keenan HA, Maddaloni E. Bone microstructure in type 1 diabetes: it's complex. Carr Osteopoulos Person in Charge (2016) 14(6):3513–8. doi: 10.1007/s11914-016-0338-8

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