![]() ![]() This will provide adequate tools to investigate the mechanism of action of drugs with potential activity in DN as well as the etiological factors in the pathogenesis of DN. The aim of this review is to highlight the available animal models and biomarkers of DN in rodents. It is important to know about the different biomarkers of neuropathy in diabetic rodents and the time it takes to develop after the induction of diabetes. Contributing factors to the neuropathy phenotype in rodents include background strain, diet composition, insulin/C-peptide deficiency, coexisting hyperglycemia and hypertension and duration of diabetes. There are advantages and disadvantages to each model for the investigation of rodent DN. The decision to select the animal model for a particular protocol is very important. Diabetic rodents show many abnormalities that are seen in diabetic patients with neuropathy, including hyperalgesia, allodynia, slow nerve conduction velocity (NCV) and progressive sensory and sensory motor deficit. The selected animal model of DN should exhibit the features present in human pathology. In order to identify new treatments of DN, it is necessary to select the precise animal model. In the United States, diabetic neuropathy (DN) is the leading cause of diabetes-related hospital admissions and nontraumatic amputations. It occurs in 60% of the patients and affects their quality of life. Neuropathy is the most common complication of diabetes mellitus (DM). Animal models and biomarkers of neuropathy in diabetic rodents. How to cite this URL: Shaikh A S, Somani R S. How to cite this article: Shaikh A S, Somani R S. Keywords: Biomarker, diabetic neuropathy, diabetic rodents ![]() We have reviewed the different animal models and biomarkers of neuropathy in diabetic rodents of either type 1 or type 2 diabetes. Diabetic rodents show behavioral, functional, structural and molecular biomarkers and they are widely used as models to investigate the etiology of DN as well as to screen the efficacy of the potential therapeutic interventions. The most useful model of DN should exhibit the key feature present in human pathology. Animal models and biomarkers of DN have been extensively used in neuropathic research. The cause of DN is still unclear and, like other complications of diabetes, it may be the result of various pathological conditions. It is a late finding in type 1 diabetes, but can be an early finding in type 2 diabetes. Together, these results provide critical characterization of disease pathogenesis in the mouse model and implicate a role for RAGE signaling as a therapeutic target to improve outcomes following SARS-CoV-2 infection.Diabetic neuropathy (DN) is a multifactor complication of diabetes. Therapeutic treatment with the RAGE antagonist FPS-ZM1 improved survival in infected mice and limited inflammation and associated perivascular pathology. Metabolic reprogramming and inflammation were initiated following this cell death event and corresponded with increased lung interstitial pneumonia, perivascular inflammation, and endothelial hyperplasia together with decreased oxygen saturation. However, a significant necrotic cell death event in CD45– populations, corresponding with peak viral loads, was observed on day 2 after infection. Early following infection, SARS-CoV-2 replicated to high titers within the lungs and evaded triggering inflammation and cell death. In this study, we temporally delineated key cell and molecular events leading to lung injury in mice following SARS-CoV-2 infection and assessed efficacy of therapeutically targeting RAGE to improve survival. The receptor for advanced glycation end products (RAGE) is a central mediator of tissue injury and contributes to SARS-CoV-2 disease pathogenesis. Cellular and molecular mechanisms driving morbidity following SARS-CoV-2 infection have not been well defined. ![]()
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