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Molecular Pharmacology in Diabetes 2.0
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Molecular Pharmacology in Diabetes 2.0

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

Deadline for manuscript submissions: 30 July 2024 | Viewed by 5462

Special Issue Editors

Dr. Rosa Fernandes

E-Mail Website
Guest Editor
Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: diabetic retinopathy; neuroinflammation; therapeutics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Flávio Reis

E-Mail Website
Guest Editor
1. Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, 3004-504 Coimbra, Portugal
2. Institute of Pharmacology & Experimental Therapeutics & Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal
Interests: gut microbiota; therapeutics & nutraceuticals; cardiovascular & metabolic disorders; renal diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetes is one of the most significant global public health concerns. Poorly controlled diabetes can have severe repercussions in a wide range of organs and tissues of the body, ranging from vascular complications, including retinopathy, nephropathy, and cardiomyopathy, to other diseases such as cancer or neurodegenerative problems. Despite advances in therapeutic strategies to lower glucose levels, some of the complications of diabetes are neither reversible nor preventable. Understanding the molecular signaling pathways underlying diabetes and related complications helps to identify potential new therapeutic targets for the management of those diseases.

This Special Issue invites important and novel advances made on the identification of key molecules and molecular signaling pathways associated with oxidative stress and inflammation in diabetes and related complications that could open new therapeutic avenues. In addition, state-of-the-art molecular studies on therapeutical options for those diseases are also welcomed, including pre-clinical studies using relevant cellular and animal models but excluding pure clinic-related research.

Dr. Rosa Fernandes
Prof. Dr. Flávio Reis
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
  • vascular complications
  • cancer
  • neurodegenerative disorders
  • key molecular players
  • signaling pathways
  • molecular biomarkers
  • pharmacological agents
  • antioxidants
  • anti-inflammatory agents

Published Papers (3 papers)

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Research

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16 pages, 2652 KiB  
Article
Improvement of Vascular Insulin Sensitivity by Ranolazine
by Sol Guerra-Ojeda, Adrian Jorda, Constanza Aldasoro, Jose M. Vila, Soraya L. Valles, Oscar J Arias-Mutis and Martin Aldasoro
Int. J. Mol. Sci. 2023, 24(17), 13532; https://doi.org/10.3390/ijms241713532 - 31 Aug 2023
Viewed by 730
Abstract
Ranolazine (RN) is a drug used in the treatment of chronic coronary ischemia. Different clinical trials have shown that RN behaves as an anti-diabetic drug by lowering blood glucose and glycosylated hemoglobin (HbA1c) levels. However, RN has not been shown to improve insulin [...] Read more.
Ranolazine (RN) is a drug used in the treatment of chronic coronary ischemia. Different clinical trials have shown that RN behaves as an anti-diabetic drug by lowering blood glucose and glycosylated hemoglobin (HbA1c) levels. However, RN has not been shown to improve insulin (IN) sensitivity. Our study investigates the possible facilitating effects of RN on the actions of IN in the rabbit aorta. IN induced vasodilation of the abdominal aorta in a concentration-dependent manner, and this dilatory effect was due to the phosphorylation of endothelial nitric oxide synthase (eNOS) and the formation of nitric oxide (NO). On the other hand, IN facilitated the vasodilator effects of acetylcholine but not the vasodilation induced by sodium nitroprusside. RN facilitated all the vasodilatory effects of IN. In addition, IN decreased the vasoconstrictor effects of adrenergic nerve stimulation and exogenous noradrenaline. Both effects were in turn facilitated by RN. The joint effect of RN with IN induced a significant increase in the ratio of p-eNOS/eNOS and pAKT/AKT. In conclusion, RN facilitated the vasodilator effects of IN, both direct and induced, on the adrenergic system. Therefore, RN increases vascular sensitivity to IN, thus decreasing tissue resistance to the hormone, a key mechanism in the development of type II diabetes. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes 2.0)
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Review

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24 pages, 2823 KiB  
Review
mTORC1 and SGLT2 Inhibitors—A Therapeutic Perspective for Diabetic Cardiomyopathy
by Sumit Saha, Xianjun Fang, Christopher D. Green and Anindita Das
Int. J. Mol. Sci. 2023, 24(20), 15078; https://doi.org/10.3390/ijms242015078 - 11 Oct 2023
Cited by 1 | Viewed by 2376
Abstract
Diabetic cardiomyopathy is a critical diabetes-mediated co-morbidity characterized by cardiac dysfunction and heart failure, without predisposing hypertensive or atherosclerotic conditions. Metabolic insulin resistance, promoting hyperglycemia and hyperlipidemia, is the primary cause of diabetes-related disorders, but ambiguous tissue-specific insulin sensitivity has shed light on [...] Read more.
Diabetic cardiomyopathy is a critical diabetes-mediated co-morbidity characterized by cardiac dysfunction and heart failure, without predisposing hypertensive or atherosclerotic conditions. Metabolic insulin resistance, promoting hyperglycemia and hyperlipidemia, is the primary cause of diabetes-related disorders, but ambiguous tissue-specific insulin sensitivity has shed light on the importance of identifying a unified target paradigm for both the glycemic and non-glycemic context of type 2 diabetes (T2D). Several studies have indicated hyperactivation of the mammalian target of rapamycin (mTOR), specifically complex 1 (mTORC1), as a critical mediator of T2D pathophysiology by promoting insulin resistance, hyperlipidemia, inflammation, vasoconstriction, and stress. Moreover, mTORC1 inhibitors like rapamycin and their analogs have shown significant benefits in diabetes and related cardiac dysfunction. Recently, FDA-approved anti-hyperglycemic sodium–glucose co-transporter 2 inhibitors (SGLT2is) have gained therapeutic popularity for T2D and diabetic cardiomyopathy, even acknowledging the absence of SGLT2 channels in the heart. Recent studies have proposed SGLT2-independent drug mechanisms to ascertain their cardioprotective benefits by regulating sodium homeostasis and mimicking energy deprivation. In this review, we systematically discuss the role of mTORC1 as a unified, eminent target to treat T2D-mediated cardiac dysfunction and scrutinize whether SGLT2is can target mTORC1 signaling to benefit patients with diabetic cardiomyopathy. Further studies are warranted to establish the underlying cardioprotective mechanisms of SGLT2is under diabetic conditions, with selective inhibition of cardiac mTORC1 but the concomitant activation of mTORC2 (mTOR complex 2) signaling. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes 2.0)
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26 pages, 1297 KiB  
Review
Immune Fingerprint in Diabetes: Ocular Surface and Retinal Inflammation
by Madania Amorim, Beatriz Martins and Rosa Fernandes
Int. J. Mol. Sci. 2023, 24(12), 9821; https://doi.org/10.3390/ijms24129821 - 06 Jun 2023
Cited by 2 | Viewed by 2018
Abstract
Diabetes is a prevalent global health issue associated with significant morbidity and mortality. Diabetic retinopathy (DR) is a well-known inflammatory, neurovascular complication of diabetes and a leading cause of preventable blindness in developed countries among working-age adults. However, the ocular surface components of [...] Read more.
Diabetes is a prevalent global health issue associated with significant morbidity and mortality. Diabetic retinopathy (DR) is a well-known inflammatory, neurovascular complication of diabetes and a leading cause of preventable blindness in developed countries among working-age adults. However, the ocular surface components of diabetic eyes are also at risk of damage due to uncontrolled diabetes, which is often overlooked. Inflammatory changes in the corneas of diabetic patients indicate that inflammation plays a significant role in diabetic complications, much like in DR. The eye’s immune privilege restricts immune and inflammatory responses, and the cornea and retina have a complex network of innate immune cells that maintain immune homeostasis. Nevertheless, low-grade inflammation in diabetes contributes to immune dysregulation. This article aims to provide an overview and discussion of how diabetes affects the ocular immune system’s main components, immune-competent cells, and inflammatory mediators. By understanding these effects, potential interventions and treatments may be developed to improve the ocular health of diabetic patients. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes 2.0)
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