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Cardiovascular Diseases: From Molecular Mechanisms to Innovative Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 September 2024) | Viewed by 1377

Special Issue Editor


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Guest Editor
Parma University Hospital, Parma, Italy
Interests: internal medicine; coagulation, statins, venous thromboembolism; pulmonary embolism; deep vein thrombosis; clotting factors; cardiovascular risk factor

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) have collectively remained the leading causes of death worldwide and substantially contribute to loss of health and excess health system costs. Therefore, numerous studies focused on etiopathogenesis, molecular diagnostic methods, and therapeutic efforts have recently been conducted.

This Special Issue on “Cardiovascular Diseases: From Molecular Mechanisms to Innovative Therapeutics” will cover a selection of the most recent scientific studies and current review articles in the field of translational and basic research dedicated to the discovery of biomarkers, molecular, and/or cellular mechanisms to be exploited as therapeutic targets or molecular diagnostic tools to improve the outcome of patients with cardiovascular disease. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Carmine Siniscalchi
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiovascular diseases
  • diabetes
  • hypertension
  • obesity
  • venous thromboembolism
  • pulmonary embolism
  • deep vein thrombosis
  • bleeding
  • coagulation
  • clotting factor

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Published Papers (1 paper)

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Research

16 pages, 5265 KiB  
Article
The Influence of Empagliflozin on the Expression of Mitochondrial Regulatory Proteins in Human Myocardium in an Ex Vivo Model of Short-Term Atrial Tachypacing
by Paweł Muszyński, Magdalena Cieślińska, Magdalena Dziemidowicz, Elżbieta Bonda-Ostaszewska, Tomasz Hirnle and Tomasz Andrzej Bonda
Int. J. Mol. Sci. 2025, 26(4), 1664; https://doi.org/10.3390/ijms26041664 - 15 Feb 2025
Viewed by 885
Abstract
Atrial fibrillation (AF) is associated with energetic deficiency and oxidative stress due to mitochondrial dysfunction, resulting in electric remodeling. Long-term treatment was found to ameliorate mitochondrial function and decrease inducibility in animal models. No studies examine the short-term effect of SGLT-2 inhibitors administration [...] Read more.
Atrial fibrillation (AF) is associated with energetic deficiency and oxidative stress due to mitochondrial dysfunction, resulting in electric remodeling. Long-term treatment was found to ameliorate mitochondrial function and decrease inducibility in animal models. No studies examine the short-term effect of SGLT-2 inhibitors administration in AF. In the present study, the samples of the right atrial appendage collected from 10 patients subjected to elective cardiac surgery were sliced and incubated in a control buffer (EMPA 0), 0.2 µmol/L empagliflozin (EMPA 0.2), or 1.0 µmol/L (EMPA 1). The expression of mitochondrial biogenesis, fission, and fusion proteins was measured by Western blot after 30 min of electrical stimulation (control—1 Hz or tachypacing—5 Hz). The PGC-1α protein expression was increased after 30 min of stimulation with 1 Hz when incubated under a higher concentration of empagliflozin. After tachypacing, EMPA 0.2 increased PGC-1α, while EMPA 1.0 upregulated NRF-1. Both concentrations increased NRF-2 during control stimulation. The oxygen consumption was higher in AF, and was decreased by SGLT-2i. Empagliflozin exerts dynamic effects on the expression of PGC-1α and other proteins involved in mitochondrial function and oxidative stress in cardiomyocytes and may modulate cellular response to tachycardia. Full article
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