Inflammatory, oxidative stress and anti-oxidative markers in patients with endometrial carcinoma and diabetes

Heidari, Firouzeh; Rabizadeh, Soghra; Mansournia, Mohammad Alì; Mirmiranpoor, Hossein; Salehi, Salome Sadat; Akhavan, Setareh; Esteghamati, Alireza; Nakhjavani, Manouchehr

doi:10.1016/j.cyto.2019.05.007

Cited by 53 publications

(42 citation statements)

References 30 publications

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“…* P < 0.05, ** P < 0.01, *** P < 0.001 vs. the control group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. the T2DM group or HG group. Recent evidence has demonstrated that increased oxidative stress and ROS are the leading causative factors driving the pathogenesis of T2DM [60][61][62] . During the development of T2DM, the cells and tissue of the body are exposed to hyperglycemic condition.…”

Section: Discussionmentioning

confidence: 99%

Acidic fibroblast growth factor attenuates type 2 diabetes-induced demyelination via suppressing oxidative stress damage

Wang

et al. 2021

Cell Death Dis

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Prolonged type 2 diabetes mellitus (T2DM) produces a common complication, peripheral neuropathy, which is accompanied by nerve fiber disorder, axon atrophy, and demyelination. Growing evidence has characterized the beneficial effects of acidic fibroblast growth factor (aFGF) and shown that it relieves hyperglycemia, increases insulin sensitivity, and ameliorates neuropathic impairment. However, there is scarce evidence on the role of aFGF on remodeling of aberrant myelin under hyperglycemia condition. Presently, we observed that the expression of aFGF was rapidly decreased in a db/db T2DM mouse model. Administration of exogenous aFGF was sufficient to block acute demyelination and nerve fiber disorganization. Furthermore, this strong anti-demyelinating effect was most likely dominated by an aFGF-mediated increase of Schwann cell (SC) proliferation and migration as well as suppression of its apoptosis. Mechanistically, the beneficial biological effects of aFGF on SC behavior and abnormal myelin morphology were likely due to the inhibition of hyperglycemia-induced oxidative stress activation, which was most likely activated by kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid-derived-like 2 (Nrf2) signaling. Thus, this evidence indicates that aFGF is a promising protective agent for relieving myelin pathology through countering oxidative stress signaling cascades under diabetic conditions.

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Section: Discussionmentioning

confidence: 99%

Acidic fibroblast growth factor attenuates type 2 diabetes-induced demyelination via suppressing oxidative stress damage

Wang

et al. 2021

Cell Death Dis

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“…Numerous studies showed that the AGEs and the advanced lipoxidation end products (ALEs) are involved in the development and progression of chronic degenerative diseases, including diabetes [28][29][30], cardiovascular diseases [29,31,32], neurological disorder [33,34], some types of cancer [35,36], and all those pathologies in which the mechanisms of oxidative stress are involved, as well as the senescence processes [33].…”

Section: Age's Biochemistrymentioning

confidence: 99%

“…The extracellular part of a RAGE molecule is composed of a variable (V-type) domain, which is followed by two constant (C-type) domains and represents the main binding sites for various ligands, while the cytosolic tail of RAGE is essential for signaling [9]. Domains of type V1 and C1 of RAGE bind a large variety of molecules ( Figure 7), not only AGEs (endogenous or food-derived) but also advanced oxidation protein products (AOPPs), involved in oxidative stress [35], β-amyloid related to Alzheimer's disease [10,74], calcium-binding S100 proteins linked to several human cancers [75], and high-mobility group box-1 (HMGB) expressed in cancer and inflammation [35,76]. RAGE receptors have been identified in a series of organs and tissues, but their highest concentration is in the lung, heart, and skeletal muscles.…”

Section: Rage: Receptor For Agesmentioning

confidence: 99%

Advanced Glycation End Products (AGEs): Biochemistry, Signaling, Analytical Methods, and Epigenetic Effects

Perrone

Giovino

Benny

et al. 2020

Oxidative Medicine and Cellular Longevity

294

219

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The advanced glycation end products (AGEs) are organic molecules formed in any living organisms with a great variety of structural and functional properties. They are considered organic markers of the glycation process. Due to their great heterogeneity, there is no specific test for their operational measurement. In this review, we have updated the most common chromatographic, colorimetric, spectroscopic, mass spectrometric, and serological methods, typically used for the determination of AGEs in biological samples. We have described their signaling and signal transduction mechanisms and cell epigenetic effects. Although mass spectrometric analysis is not widespread in the detection of AGEs at the clinical level, this technique is highly promising for the early diagnosis and therapeutics of diseases caused by AGEs. Protocols are available for high-resolution mass spectrometry of glycated proteins although they are characterized by complex machine management. Simpler procedures are available although much less precise than mass spectrometry. Among them, immunochemical tests are very common since they are able to detect AGEs in a simple and immediate way. In these years, new methodologies have been developed using an in vivo novel and noninvasive spectroscopic methods. These methods are based on the measurement of autofluorescence of AGEs. Another method consists of detecting AGEs in the human skin to detect chronic exposure, without the inconvenience of invasive methods. The aim of this review is to compare the different approaches of measuring AGEs at a clinical perspective due to their strict association with oxidative stress and inflammation.

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“…It has been shown that RAGE does not only recognize AGEs (endogenous or food-derived), but also other compounds, e.g., advanced protein oxidation products (engaged in oxidative stress), fibrillar β-sheet forming amyloids characteristic of Alzheimer's disease [84], S100 protein family members (Ca 2+ -binding modulators), and high mobility group box-1 (expressed in cancer) (Figure 2). AGE-RAGE interaction evokes constant and strong cellular response, inducing an intracellular cascade of inflammatory reactions which lead to release of proinflammatory cytokines [85], intensification of oxidative stress, increased risk of coagulopathies [86], overexpression of different extracellular matrix proteins (such as collagen or laminin) [87], and activation of secondary signal transmitters, e.g., kinase C. These processes promote alterations in cellular stimulation, migration, and proliferation, leading to pathological condition such as diabetic complications, sclerosis, Alzheimer's disease, inflammation, and tumor development [88]. Most of these conditions are due to RAGE-associated release of intermediates of various cell signaling pathways, such as ROS, p21ras, erk1/2 (p44/p42), MAPK kinase [89] p38, SAPK/JNK MAP kinases, rhoGTPases, phosphoinositol-3 kinase, and intermediates of JAK/STAT pathway.…”

Section: The Glycation Process Advanced Glycation End-products and Their Receptorsmentioning

confidence: 99%

Role of Advanced Glycation End-Products and Other Ligands for AGE Receptors in Thyroid Cancer Progression

Bronowicka-Szydełko

Kotyra

Lewandowski

et al. 2021

JCM

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To date, thyroid cancers (TCs) remain a clinical challenge owing to their heterogeneous nature. The etiopathology of TCs is associated not only with genetic mutations or chromosomal rearrangements, but also non-genetic factors, such as oxidative-, nitrosative-, and carbonyl stress-related alterations in tumor environment. These factors, through leading to the activation of intracellular signaling pathways, induce tumor tissue proliferation. Interestingly, the incidence of TCs is often coexistent with various simultaneous mutations. Advanced glycation end-products (AGEs), their precursors and receptors (RAGEs), and other ligands for RAGEs are reported to have significant influence on carcinogenesis and TCs progression, inducing gene mutations, disturbances in histone methylation, and disorders in important carcinogenesis-related pathways, such as PI3K/AKT/NF-kB, p21/MEK/MPAK, or JAK/STAT, RAS/ERK/p53, which induce synthesis of interleukins, growth factors, and cytokines, thus influencing metastasis, angiogenesis, and cancer proliferation. Precursors of AGE (such as methylglyoxal (MG)) and selected ligands for RAGEs: AS1004, AS1008, and HMGB1 may, in the future, become potential targets for TCs treatment, as low MG concentration is associated with less aggressive anaplastic thyroid cancer, whereas the administration of anti-RAGE antibodies inhibits the progression of papillary thyroid cancer and anaplastic thyroid cancer. This review is aimed at collecting the information on the role of compounds, engaged in glycation process, in the pathogenesis of TCs. Moreover, the utility of these compounds in the diagnosis and treatment of TCs is thoroughly discussed. Understanding the mechanism of action of these compounds on TCs pathogenesis and progression may potentially be the grounds for the development of new treatment strategies, aiming at quality-of-life improvements.

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Inflammatory, oxidative stress and anti-oxidative markers in patients with endometrial carcinoma and diabetes

Cited by 53 publications

References 30 publications

Acidic fibroblast growth factor attenuates type 2 diabetes-induced demyelination via suppressing oxidative stress damage

Acidic fibroblast growth factor attenuates type 2 diabetes-induced demyelination via suppressing oxidative stress damage

Advanced Glycation End Products (AGEs): Biochemistry, Signaling, Analytical Methods, and Epigenetic Effects

Role of Advanced Glycation End-Products and Other Ligands for AGE Receptors in Thyroid Cancer Progression

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