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Cell Biology in Diabetes and Diabetic Complications
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Cell Biology in Diabetes and Diabetic Complications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 7876

Special Issue Editors

Dr. Paola Pontrelli

E-Mail Website
Guest Editor
Nephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, 70124 Bari, Italy
Interests: genomics; transcriptomics; diabetic nephropathy; kidney transplantation
Special Issues, Collections and Topics in MDPI journals
Dr. Francesca Conserva

E-Mail Website
Guest Editor
Nephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, 70124 Bari, Italy
Interests: kidney; biomarker; nephropathy; diabetes

Special Issue Information

Dear Colleagues,

Diabetes is a chronic, multifactorial disease, and its related micro- and macrovascular complications are particularly relevant due to the devastating effects that disease progression has both on patients and healthcare systems worldwide. The most common diabetes-related diseases include cardiovascular diseases, diabetic neuropathy, diabetic retinopathy, and diabetic nephropathy, among others, thus affecting the physiology of different cells and tissues. Moreover, obesity, insulin resistance, hypertension, and genetic predisposition can contribute to disease progression.

In the present Special Issue entitled "Cell Biology in Diabetes and Diabetic Complications", we will cover the current research efforts on the molecular mechanisms that drive cellular dysfunction and organ failure in patients with diabetes. We will include papers discussing prevention, general pathophysiology, and novel frontiers in the treatment of diabetes and its complications.

Subtopics will include but will not be limited to:

  • High-glucose-induced metabolic changes that drive hypoxia, promote senescence, and alter cell fate;
  • Epigenetics and RNA mediated mechanisms of disease in type 1 and type 2 diabetes and diabetes complications;
  • Recent advances in the characterization of the molecular features that promote vascular damage, inflammation, and fibrosis;
  • Novel underlying mechanisms responsible for the development of diabetes complications, such as diabetic nephropathy, retinopathy, and cardiovascular disease;
  • Relevant discoveries on the mechanisms of action of established and novel drugs in diabetes management.

Dr. Paola Pontrelli
Dr. Francesca Conserva
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • obesity
  • insulin resistance
  • hypertension
  • diabetic nephropathy

Published Papers (4 papers)

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Research

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35 pages, 15542 KiB  
Article
Antidiabetic and Immunoregulatory Activities of Extract of Phyllanthus emblica L. in NOD with Spontaneous and Cyclophosphamide-Accelerated Diabetic Mice
by Cheng-Hsiu Lin, Yueh-Hsiung Kuo and Chun-Ching Shih
Int. J. Mol. Sci. 2023, 24(12), 9922; https://doi.org/10.3390/ijms24129922 - 08 Jun 2023
Cited by 2 | Viewed by 1525
Abstract
Oil-Gan, also known as emblica, is the fruit of the genus Phyllanthus emblica L. The fruits are high in nutrients and display excellent health care functions and development values. The primary aim of this study was to investigate the activities of ethyl acetate [...] Read more.
Oil-Gan, also known as emblica, is the fruit of the genus Phyllanthus emblica L. The fruits are high in nutrients and display excellent health care functions and development values. The primary aim of this study was to investigate the activities of ethyl acetate extract from Phyllanthus emblica L. (EPE) on type 1 diabetes mellitus (T1D) and immunoregulatory activities in non-obese diabetes (NOD) mice with spontaneous and cyclophosphamide (Cyp)-accelerated diabetes. EPE was vehicle-administered to spontaneous NOD (S-NOD) mice or Cyp-accelerated NOD (Cyp-NOD) mice once daily at a dose of 400 mg/kg body weight for 15 or 4 weeks, respectively. At the end, blood samples were collected for biological analyses, organ tissues were dissected for analyses of histology and immunofluorescence (IF) staining (including expressions of Bcl and Bax), the expression levels of targeted genes by Western blotting and forkhead box P3 (Foxp3), and helper T lymphocyte 1 (Th1)/Th2/Th17/Treg regulatory T cell (Treg) cell distribution by flow cytometry. Our results showed that EPE-treated NOD mice or Cyp-accelerated NOD mice display a decrease in levels of blood glucose and HbA1c, but an increase in blood insulin levels. EPE treatment decreased blood levels of IFN-γ and tumor necrosis α (TNF-α) by Th1 cells, and reduced interleukin (IL)-1β and IL-6 by Th17 cells, but increased IL-4, IL-10, and transforming growth factor-β1 (TGF-β1) by Th2 cells in both of the two mice models by enzyme-linked immunosorbent assay (ELISA) analysis. Flow cytometric data showed that EPE-treated Cyp-NOD mice had decreased the CD4+ subsets T cell distribution of CD4+IL-17 and CD4+ interferon gamma (IFN-γ), but increased the CD4+ subsets T cell distribution of CD4+IL-4 and CD4+Foxp3. Furthermore, EPE-treated Cyp-NOD mice had decreased the percentage per 10,000 cells of CD4+IL-17 and CD4+IFNγ, and increased CD4+IL-4 and CD4+Foxp3 compared with the Cyp-NOD Con group (p < 0.001, p < 0.05, p < 0.05, and p < 0.05, respectively). For target gene expression levels in the pancreas, EPE-treated mice had reduced expression levels of inflammatory cytokines, including IFN-γ and TNF-α by Th1 cells, but increased expression levels of IL-4, IL-10, and TGF-1β by Th2 cells in both two mice models. Histological examination of the pancreas revealed that EPE-treated mice had not only increased pancreatic insulin-expressing β cells (brown), and but also enhanced the percentage of Bcl-2 (green)/Bax (red) by IF staining analyses of islets compared with the S-NOD Con and the Cyp-NOD Con mice, implying that EPE displayed the protective effects of pancreas β cells. EPE-treated mice showed an increase in the average immunoreactive system (IRS) score on insulin within the pancreas, and an enhancement in the numbers of the pancreatic islets. EPE displayed an improvement in the pancreas IRS scores and a decrease in proinflammatory cytokines. Moreover, EPE exerted blood-glucose-lowering effects by regulating IL-17 expressions. Collectively, these results implied that EPE inhibits the development of autoimmune diabetes by regulating cytokine expression. Our results demonstrated that EPE has a therapeutic potential in the preventive effects of T1D and immunoregulation as a supplementary. Full article
(This article belongs to the Special Issue Cell Biology in Diabetes and Diabetic Complications)
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15 pages, 7887 KiB  
Article
Argonaute 2 Restores Erectile Function by Enhancing Angiogenesis and Reducing Reactive Oxygen Species Production in Streptozotocin (STZ)-Induced Type-1 Diabetic Mice
by Fang-Yuan Liu, Guo Nan Yin, Jiyeon Ock, Fitri Rahma Fridayana, Lashkari Niloofar, Yan Huang, Minh Nhat Vo, Jun-Kyu Suh, Soon-Sun Hong, Ju-Hee Kang and Ji-Kan Ryu
Int. J. Mol. Sci. 2023, 24(3), 2935; https://doi.org/10.3390/ijms24032935 - 02 Feb 2023
Cited by 1 | Viewed by 2130
Abstract
Severe vascular and nerve damage from diabetes is a leading cause of erectile dysfunction (ED) and poor response to oral phosphodiesterase 5 inhibitors. Argonaute 2 (Ago2), a catalytic engine in mammalian RNA interference, is involved in neurovascular regeneration under inflammatory conditions. In the [...] Read more.
Severe vascular and nerve damage from diabetes is a leading cause of erectile dysfunction (ED) and poor response to oral phosphodiesterase 5 inhibitors. Argonaute 2 (Ago2), a catalytic engine in mammalian RNA interference, is involved in neurovascular regeneration under inflammatory conditions. In the present study, we report that Ago2 administration can effectively improve penile erection by enhancing cavernous endothelial cell angiogenesis and survival under diabetic conditions. We found that although Ago2 is highly expressed around blood vessels and nerves, it is significantly reduced in the penis tissue of diabetic mice. Exogenous administration of the Ago2 protein restored erectile function in diabetic mice by reducing reactive oxygen species production-signaling pathways (inducing eNOS Ser1177/NF-κB Ser536 signaling) and improving cavernous endothelial angiogenesis, migration, and cell survival. Our study provides new evidence that Ago2 mediation may be a promising therapeutic strategy and a new approach for diabetic ED treatment. Full article
(This article belongs to the Special Issue Cell Biology in Diabetes and Diabetic Complications)
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18 pages, 5552 KiB  
Article
SENP6-Mediated deSUMOylation of VEGFR2 Enhances Its Cell Membrane Transport in Angiogenesis
by Qi He, Zhenfeng Chen, Jieyu Li, Jinlian Liu, Zirui Zuo, Bingqi Lin, Ke Song, Chuyu Zhou, Haipeng Lai, Qiaobing Huang and Xiaohua Guo
Int. J. Mol. Sci. 2023, 24(3), 2544; https://doi.org/10.3390/ijms24032544 - 29 Jan 2023
Cited by 2 | Viewed by 2340
Abstract
Angiogenesis is a significant pathogenic characteristic of diabetic microangiopathy. Advanced glycation end products (AGEs) are considerably elevated in diabetic tissues and can affect vascular endothelial cell shape and function. Regulation of the vascular endothelial growth factor (VEGF)-VEGF receptor 2 (VEGFR2) signaling pathway is [...] Read more.
Angiogenesis is a significant pathogenic characteristic of diabetic microangiopathy. Advanced glycation end products (AGEs) are considerably elevated in diabetic tissues and can affect vascular endothelial cell shape and function. Regulation of the vascular endothelial growth factor (VEGF)-VEGF receptor 2 (VEGFR2) signaling pathway is a critical mechanism in the regulation of angiogenesis, and VEGFR2 activity can be modified by post-translational changes. However, little research has been conducted on the control of small ubiquitin-related modifier (SUMO)-mediated VEGFR2 alterations. The current study investigated this using human umbilical vein endothelial cells (HUVECs) in conjunction with immunoblotting and immunofluorescence. AGEs increased Nrf2 translocation to the nucleus and promoted VEGFR2 expression. They also increased the expression of sentrin/SUMO-specific protease 6 (SENP6), which de-SUMOylated VEGFR2, and immunofluorescence indicated a reduction in VEGFR2 accumulation in the Golgi and increased VEGFR2 transport from the Golgi to the cell membrane surface via the coatomer protein complex subunit beta 2. VEGFR2 on the cell membrane was linked to VEGF generated by pericytes, triggering the VEGF signaling cascade. In conclusion, this study demonstrates that SENP6 regulates VEGFR2 trafficking from the Golgi to the endothelial cell surface. The SENP6-VEGFR2 pathway plays a critical role in pathological angiogenesis. Full article
(This article belongs to the Special Issue Cell Biology in Diabetes and Diabetic Complications)
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Review

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16 pages, 688 KiB  
Review
The p66Shc Redox Protein and the Emerging Complications of Diabetes
by Giuseppina Biondi, Nicola Marrano, Anna Borrelli, Martina Rella, Rossella D’Oria, Valentina Annamaria Genchi, Cristina Caccioppoli, Angelo Cignarelli, Sebastio Perrini, Luigi Laviola, Francesco Giorgino and Annalisa Natalicchio
Int. J. Mol. Sci. 2024, 25(1), 108; https://doi.org/10.3390/ijms25010108 - 20 Dec 2023
Viewed by 1219
Abstract
Diabetes mellitus is a chronic metabolic disease, the prevalence of which is constantly increasing worldwide. It is often burdened by disabling comorbidities that reduce the quality and expectancy of life of the affected individuals. The traditional complications of diabetes are generally described as [...] Read more.
Diabetes mellitus is a chronic metabolic disease, the prevalence of which is constantly increasing worldwide. It is often burdened by disabling comorbidities that reduce the quality and expectancy of life of the affected individuals. The traditional complications of diabetes are generally described as macrovascular complications (e.g., coronary heart disease, peripheral arterial disease, and stroke), and microvascular complications (e.g., diabetic kidney disease, retinopathy, and neuropathy). Recently, due to advances in diabetes management and the increased life expectancy of diabetic patients, a strong correlation between diabetes and other pathological conditions (such as liver diseases, cancer, neurodegenerative diseases, cognitive impairments, and sleep disorders) has emerged. Therefore, these comorbidities have been proposed as emerging complications of diabetes. P66Shc is a redox protein that plays a role in oxidative stress, apoptosis, glucose metabolism, and cellular aging. It can be regulated by various stressful stimuli typical of the diabetic milieu and is involved in various types of organ and tissue damage under diabetic conditions. Although its role in the pathogenesis of diabetes remains controversial, there is strong evidence regarding the involvement of p66Shc in the traditional complications of diabetes. In this review, we will summarize the evidence supporting the role of p66Shc in the pathogenesis of diabetes and its complications, focusing for the first time on the emerging complications of diabetes. Full article
(This article belongs to the Special Issue Cell Biology in Diabetes and Diabetic Complications)
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