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Roles of Diabetes in Cardiovascular Disorders and Nephropathy

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A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (6 February 2023) | Viewed by 6030

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Special Issue Editors

Dr. Vivek Pandey

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Guest Editor

Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA
Interests: diabetic cardiomyopathies; diabetic nephropathy; oxidative stress; transporter proteins; cell signaling; ER stress; phytochemicals

Dr. Sanjay Saini

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Guest Editor

Physiology and Cellular Biophysics, Columbia University Irving Medical Center, New York, NY, USA
Interests: diabetic nephropathy; cell signaling; molecular biology

Dr. Arjun Singh

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Guest Editor

Molecular Pharmacology Program, Laboratory of Signal Transduction, Mortimer B. Zuckerman Research Center, 417 East 68th Street, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Interests: molecular pharmacology; cancer pharmacology; natural products; ethnomedicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) and chronic kidney damages are the major risk factors associated with diabetes. Recent research has established the fact that diabetic patients with kidney diseases have higher risks for heart failure/CVD. Decreased estimated glomerular filtration rate and increased albuminuria are considered independent risk factors for cardiovascular mortality in patients. Link/competition between end-stage renal disease (ESRD) and CVD worsens diabetic pathophysiology. Diabetes enhances the risk of ESRD by manifolds in patients leading to chronic kidney diseases. Moreover, inhibition of SGLT2 in kidneys is proven to show beneficial effects on the hearts. Mechanisms regulating the etiology of the trilogy of diabetes, cardiovascular disorders, and nephropathy is not known. Articles focused on understanding the pathophysiology of heart and kidney diseases and/or their synergistic effects during diabetes are welcome in this Special Issue.

Specific aims of the issue:

To publish original research, review articles and commentaries on the below topics:

the role of diabetes (T1D, T2D, maternal diabetes) in cardiovascular diseases and nephropathy: this may include studies on specific cellular signaling pathways, treatment approaches, and phytochemicals used to manage the adverse effects of the disease;
mitochondrial bioenergetics in diabetic cardiomyopathies and nephropathies.;
endoplasmic reticulum (ER) stress in the progression of in diabetic cardiomyopathies and nephropathies;
the effect of oxidative stress on post-translational modifications regulating diabetic cardiovascular disorders and nephropathy;
membrane protein/transporter protein regulation during diabetic heart and kidney diseases;
plant products/bioactive compounds regulating the cellular mechanisms during diabetic cardiomyopathy and/or nephropathy.

Dr. Vivek Kumar Pandey
Dr. Sanjay Saini
Dr. Arjun Singh
Guest Editors

Manuscript Submission Information

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Keywords

diabetes
heart
kidney
cardiomyopathy
nephropathy
ER stress
oxidative stress
ESRD
CKD
CVD

Published Papers (2 papers)

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Research

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14 pages, 2870 KiB

Open AccessArticle

Capsaicin Ameliorates the Cyclophosphamide-Induced Cardiotoxicity by Inhibiting Free Radicals Generation, Inflammatory Cytokines, and Apoptotic Pathway in Rats

by Rayan A. Ahmed, Mohammad Firoz Alam, Saeed Alshahrani, Abdulmajeed M. Jali, Abdullah M. Qahl, Mohammad Khalid, Hisham M. A. Muzafar, Hussain N. Alhamami and Tarique Anwer

Life 2023, 13(3), 786; https://doi.org/10.3390/life13030786 - 14 Mar 2023

Cited by 3 | Viewed by 1950

Abstract

Cyclophosphamide is an antineoplastic agent that has a broad range of therapeutic applications; however, it has numerous side effects, including cardiotoxicity. Furthermore, chili peppers contain a substance called capsaicin, having antioxidant and anti-inflammatory effects. Thus, this research paper focuses on the potential mechanism of capsaicin’s cardioprotective activity against cyclophosphamide-induced cardiotoxicity by measuring the expression of oxidative and inflammatory marker such as interleukins and caspases. The following groups of rats were randomly assigned: only vehicle given for 6 days (control group); cyclophosphamide 200 mg/kg intraperitoneal on 4th day only (positive control group); capsaicin 10 mg/kg orally given for 6 days followed by cyclophosphamide 200 mg/kg on 4th day of treatment; capsaicin 20 mg/kg orally for six days followed by cyclophosphamide 200 mg/kg on 4th day of treatment; and maximum amount of capsaicin alone (20 mg/kg) orally for six days. Using ELISA kits, it was found that the cyclophosphamide administration significantly increased the levels of lactate dehydrogenase, troponin-I (cardiac cell damage marker), lipid peroxidation, triglyceride, interleukin-6, tumor necrosis factor-alpha, and caspase 3. However, it markedly reduced the antioxidant enzymes catalase and glutathione levels. Both doses of capsaicin could reverse cardiac cell damage markers, as shown by a significant decline in (lactate dehydrogenase and troponin-I). In addition, capsaicin significantly reduced the cytokine levels (interleukin-6 and tumor necrosis factor-alpha), caspase 3, lipid peroxidation, and triglycerides. However, capsaicin treatment significantly raised the antioxidant content of enzymes such as glutathione and catalase. The capsaicin-treated group restored the oxidative parameter’s imbalance and generated considerable protection against cardiomyocyte harm from cyclophosphamide in male Wistar rats. These protective effects might be beneficial against the negative impacts of cyclophosphamide when used to treat cancer and immune-mediated diseases. Full article

(This article belongs to the Special Issue Roles of Diabetes in Cardiovascular Disorders and Nephropathy)

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Review

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32 pages, 2028 KiB

Open AccessReview

Anti-Diabetic Therapy and Heart Failure: Recent Advances in Clinical Evidence and Molecular Mechanism

by Chih-Neng Hsu, Chin-Feng Hsuan, Daniel Liao, Jack Keng-Jui Chang, Allen Jiun-Wei Chang, Siow-Wey Hee, Hsiao-Lin Lee and Sean I. F. Teng

Life 2023, 13(4), 1024; https://doi.org/10.3390/life13041024 - 16 Apr 2023

Cited by 1 | Viewed by 3597

Abstract

Diabetic patients have a two- to four-fold increase in the risk of heart failure (HF), and the co-existence of diabetes and HF is associated with poor prognosis. In randomized clinical trials (RCTs), compelling evidence has demonstrated the beneficial effects of sodium-glucose co-transporter-2 inhibitors on HF. The mechanism includes increased glucosuria, restored tubular glomerular feedback with attenuated renin–angiotensin II–aldosterone activation, improved energy utilization, decreased sympathetic tone, improved mitochondria calcium homeostasis, enhanced autophagy, and reduced cardiac inflammation, oxidative stress, and fibrosis. The RCTs demonstrated a neutral effect of the glucagon-like peptide receptor agonist on HF despite its weight-reducing effect, probably due to it possibly increasing the heart rate via increasing cyclic adenosine monophosphate (cAMP). Observational studies supported the markedly beneficial effects of bariatric and metabolic surgery on HF despite no current supporting evidence from RCTs. Bromocriptine can be used to treat peripartum cardiomyopathy by reducing the harmful cleaved prolactin fragments during late pregnancy. Preclinical studies suggest the possible beneficial effect of imeglimin on HF through improving mitochondrial function, but further clinical evidence is needed. Although abundant preclinical and observational studies support the beneficial effects of metformin on HF, there is limited evidence from RCTs. Thiazolidinediones increase the risk of hospitalized HF through increasing renal tubular sodium reabsorption mediated via both the genomic and non-genomic action of PPARγ. RCTs suggest that dipeptidyl peptidase-4 inhibitors, including saxagliptin and possibly alogliptin, may increase the risk of hospitalized HF, probably owing to increased circulating vasoactive peptides, which impair endothelial function, activate sympathetic tones, and cause cardiac remodeling. Observational studies and RCTs have demonstrated the neutral effects of insulin, sulfonylureas, an alpha-glucosidase inhibitor, and lifestyle interventions on HF in diabetic patients. Full article

(This article belongs to the Special Issue Roles of Diabetes in Cardiovascular Disorders and Nephropathy)

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