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Biomedicines
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Molecular Insights into Myocardial Infarction
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Molecular Insights into Myocardial Infarction

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 7030

Special Issue Editor

Dr. Dong Wang

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA
Interests: cardiovascular disease; myocardial infarction; cell death; fibroblast; heart failure; ischemic stroke; atrial thrombosis

Special Issue Information

Dear Colleagues,

Myocardial infarction, commonly known as a heart attack, is a leading cause of morbidity and mortality worldwide. Recent advancements in molecular research have provided valuable insights into the pathogenesis, diagnosis, and treatment of myocardial infarction. This Special Issue aims to explore the latest discoveries and breakthroughs in the field of molecular cardiology, specifically focusing on the molecular mechanisms underlying myocardial infarction.

The scope of this Special Issue covers a wide range of topics, including (but not limited to) the following:

  1. The identification and characterization of molecular markers for the early diagnosis and risk stratification of myocardial infarction;
  2. Understanding the role of genetic variations and epigenetic modifications in myocardial infarction susceptibility and progression;
  3. The exploration of molecular pathways involved in myocardial ischemia–reperfusion injury and myocardial remodeling;
  4. Novel therapeutic targets and strategies based on molecular insights for the prevention and treatment of myocardial infarction;
  5. Advancements in molecular imaging techniques for the assessment of myocardial infarction and monitoring treatment response;
  6. The integration of omics approaches (genomics, transcriptomics, proteomics, and metabolomics) to unravel the complex molecular networks associated with myocardial infarction.

We invite you, researchers, and scientists from diverse disciplines to contribute your original research, reviews, and perspectives to this Special Issue. By collectively sharing and discussing the latest molecular insights, we aim to deepen our understanding of myocardial infarction and pave the way for innovative diagnostic tools and targeted therapies.

Dr. Dong Wang
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • myocardial infarction
  • molecular markers
  • molecular pathways
  • gene expression
  • epigenetic modifications
  • transcriptomics
  • metabolomics
  • proteomics
  • cell death
  • cell survival
  • cardiac remodeling

Published Papers (7 papers)

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Research

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13 pages, 3661 KiB  
Article
Proteomic Profiling of SGLT-2 Inhibitor Canagliflozin in a Swine Model of Chronic Myocardial Ischemia
by Dwight D. Harris, Sharif A. Sabe, Mark Broadwin, Christopher Stone, Cynthia Xu, Jiayu Hu, Meghamsh Kanuparthy, M. Ruhul Abid and Frank W. Sellke
Biomedicines 2024, 12(3), 588; https://doi.org/10.3390/biomedicines12030588 - 06 Mar 2024
Viewed by 673
Abstract
Background: Sodium–glucose cotransporter-2 (SGLT2) inhibitors are known to be cardioprotective independent of glucose control, but the mechanisms of these benefits are unclear. We previously demonstrated improved cardiac function and decreased fibrosis in a swine model of chronic myocardial ischemia. The goal of this [...] Read more.
Background: Sodium–glucose cotransporter-2 (SGLT2) inhibitors are known to be cardioprotective independent of glucose control, but the mechanisms of these benefits are unclear. We previously demonstrated improved cardiac function and decreased fibrosis in a swine model of chronic myocardial ischemia. The goal of this study is to use high-sensitivity proteomic analyses to characterize specific molecular pathways affected by SGLT-2 inhibitor canagliflozin (CAN) therapy in a swine model of chronic myocardial ischemia. Methods: Chronic myocardial ischemia was induced in sixteen Yorkshire swine via the placement of an ameroid constrictor to the left circumflex coronary artery. After two weeks of recovery, swine received either 300 mg of CAN daily (n = 8) or a control (n = 8). After five weeks of therapy, the group of swine were euthanized, and left ventricular tissue was harvested and sent for proteomic analysis. Results: Total proteomic analysis identified a total of 3256 proteins between the CAN and control groups. Three hundred and five proteins were statistically different. This included 55 proteins that were downregulated (p < 0.05, fold change <0.5) and 250 that were upregulated (p < 0.05, fold change >2) with CAN treatment. Pathway analysis demonstrated the upregulation of several proteins involved in metabolism and redox activity in the CAN-treated group. The CAN group also exhibited a downregulation of proteins involved in motor activity and cytoskeletal structure. Conclusions: In our swine model of chronic myocardial ischemia, CAN therapy alters several proteins involved in critical molecular pathways, including redox regulation and metabolism. These findings provide additional mechanistic insights into the cardioprotective effects of canagliflozin. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
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12 pages, 689 KiB  
Article
Influence of Obesity on Short-Term Surgical Outcomes in HFrEF Patients Undergoing CABG: A Retrospective Multicenter Study
by Christian Jörg Rustenbach, Stefan Reichert, Christoph Salewski, Julia Schano, Rafal Berger, Attila Nemeth, Monika Zdanyte, Helene Häberle, Túlio Caldonazo, Ibrahim Saqer, Shekhar Saha, Philipp Schnackenburg, Ilija Djordjevic, Ihor Krasivskyi, Lina María Serna-Higuita, Torsten Doenst, Christian Hagl, Thorsten Wahlers, Christian Schlensak and Rodrigo Sandoval Boburg
Biomedicines 2024, 12(2), 426; https://doi.org/10.3390/biomedicines12020426 - 13 Feb 2024
Viewed by 826
Abstract
Background: This retrospective multicenter study investigates the impact of obesity on short-term surgical outcomes in patients with heart failure and reduced ejection fraction (HFrEF) undergoing coronary artery bypass grafting (CABG). Given the rising global prevalence of obesity and its known cardiovascular implications, [...] Read more.
Background: This retrospective multicenter study investigates the impact of obesity on short-term surgical outcomes in patients with heart failure and reduced ejection fraction (HFrEF) undergoing coronary artery bypass grafting (CABG). Given the rising global prevalence of obesity and its known cardiovascular implications, understanding its specific effects in high-risk groups like HFrEF patients is crucial. Methods: The study analyzed data from 574 patients undergoing CABG across four German university hospitals from 2017 to 2023. Patients were stratified into ‘normal weight’ (n = 163) and ‘obese’ (n = 158) categories based on BMI (WHO classification). Data on demographics, clinical measurements, health status, cardiac history, intraoperative management, postoperative outcomes, and laboratory insights were collected and analyzed using Chi-square, ANOVA, Kruskal–Wallis, and binary logistic regression. Results: Key findings are a significant higher mortality rate (6.96% vs. 3.68%, p = 0.049) and younger age in obese patients (mean age 65.84 vs. 69.15 years, p = 0.003). Gender distribution showed no significant difference. Clinical assessment scores like EuroScore II and STS Score indicated no differences. Paradoxically, the preoperative left ventricular ejection fraction (LVEF) was higher in the obese group (32.04% vs. 30.34%, p = 0.026). The prevalence of hypertension, COPD, hyperlipidemia, and other comorbidities did not significantly differ. Intraoperatively, obese patients required more packed red blood cells (p = 0.026), indicating a greater need for transfusion. Postoperatively, the obese group experienced longer hospital stays (median 14 vs. 13 days, p = 0.041) and higher ventilation times (median 16 vs. 13 h, p = 0.049). The incidence of acute kidney injury (AKI) (17.72% vs. 9.20%, p = 0.048) and delirium (p = 0.016) was significantly higher, while, for diabetes prevalence, there was an indicating a trend towards significance (p = 0.051) in the obesity group, while other complications like sepsis, and the need for ECLS were similar across groups. Conclusions: The study reveals that obesity significantly worsens short-term outcomes in HFrEF patients undergoing CABG, increasing risks like mortality, kidney insufficiency, and postoperative delirium. These findings highlight the urgent need for personalized care, from surgical planning to postoperative strategies, to improve outcomes for this high-risk group, urging further tailored research. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
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15 pages, 1925 KiB  
Article
On- vs. Off-Pump CABG in Heart Failure Patients with Reduced Ejection Fraction (HFrEF): A Multicenter Analysis
by Christian Jörg Rustenbach, Stefan Reichert, Medhat Radwan, Isabelle Doll, Migdat Mustafi, Attila Nemeth, Spiros Lukas Marinos, Rafal Berger, Hardy Baumbach, Monika Zdanyte, Helene Haeberle, Tulio Caldonazo, Ibrahim Saqer, Shekhar Saha, Philipp Schnackenburg, Ilija Djordjevic, Ihor Krasivskyi, Stefanie Wendt, Elmar Kuhn, Lina Maria Serna Higuita, Torsten Doenst, Christian Hagl, Thorsten Wahlers, Rodrigo Sandoval Boburg and Christian Schlensakadd Show full author list remove Hide full author list
Biomedicines 2023, 11(11), 3043; https://doi.org/10.3390/biomedicines11113043 - 14 Nov 2023
Cited by 2 | Viewed by 1120
Abstract
Objective: This study aimed to compare postoperative outcomes and 30-day mortality in patients with reduced ejection fraction (<40%) who underwent isolated coronary artery bypass grafting (CABG) with (ONCAB) and without (OPCAB) the use of cardiopulmonary bypass. Methods: data from four university hospitals in [...] Read more.
Objective: This study aimed to compare postoperative outcomes and 30-day mortality in patients with reduced ejection fraction (<40%) who underwent isolated coronary artery bypass grafting (CABG) with (ONCAB) and without (OPCAB) the use of cardiopulmonary bypass. Methods: data from four university hospitals in Germany, spanning from January 2017 to December 2021, were retrospectively analyzed. A total of 551 patients were included in the study, and various demographic, intraoperative, and postoperative data were compared. Results: demographic parameters did not exhibit any differences. However, the OPCAB group displayed notably higher rates of preoperative renal insufficiency, urgent surgeries, and elevated EuroScore II and STS score. During surgery, the ONCAB group showed a significantly higher rate of complete revascularization, whereas the OPCAB group required fewer intraoperative transfusions. No disparities were observed in 30-day/in-hospital mortality for the entire cohort and the matched population between the two groups. Subsequent to surgery, the OPCAB group demonstrated significantly shorter mechanical ventilation times, reduced stays in the intensive care unit, and lower occurrences of ECLS therapy, acute kidney injury, delirium, and sepsis. Conclusions: the study’s findings indicate that OPCAB surgery presents a safe and viable alternative, yielding improved postoperative outcomes in this specific patient population compared to ONCAB surgery. Despite comparable 30-day/in-hospital mortality rates, OPCAB patients enjoyed advantages such as decreased mechanical ventilation durations, shorter ICU stays, and reduced incidences of ECLS therapy, acute kidney injury, delirium, and sepsis. These results underscore the potential benefits of employing OPCAB as a treatment approach for patients with coronary heart disease and reduced ejection fraction. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
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13 pages, 2614 KiB  
Article
Transcriptional Activity of Metalloproteinase 9 (MMP-9) and Tissue Metalloproteinase 1 (TIMP-1) Genes as a Diagnostic and Prognostic Marker of Heart Failure Due to Ischemic Heart Disease
by Dariusz Korzeń, Oskar Sierka and Józefa Dąbek
Biomedicines 2023, 11(10), 2776; https://doi.org/10.3390/biomedicines11102776 - 13 Oct 2023
Cited by 3 | Viewed by 710
Abstract
The most common cause of heart failure (HF) is coronary artery disease (CAD). The aim of this study was to evaluate the transcriptional activity of the metalloproteinase 9 (MMP-9) and tissue metalloproteinase inhibitor 1 (TIMP-1) genes in a study [...] Read more.
The most common cause of heart failure (HF) is coronary artery disease (CAD). The aim of this study was to evaluate the transcriptional activity of the metalloproteinase 9 (MMP-9) and tissue metalloproteinase inhibitor 1 (TIMP-1) genes in a study group of patients with HF due to CAD and in the control group, as well as assess the transcriptional activity of the examined genes, taking into account the number of affected coronary arteries and the severity of heart failure. The study group consisted of a total of 150 (100%) patients. The material for the study was peripheral blood, and molecular tests were performed using the quantitative QRT-PCR technique. The transcriptional activity of the MMP-9 gene was significantly higher in the group of patients with CAD and HF. It was also significantly higher with the progression of heart failure. TIMP-1 gene transcriptional activity was significantly lower with the advancement of heart failure. The transcriptional activity of the MMP-9 and TIMP-1 genes differentiated the examined patients. The severity of HF, and a significant increase in the QRT-PCR transcriptional activity of the MMP-9 gene with a simultaneous decrease in the activity of the TIMP-1 gene, makes them useful diagnostic and prognostic markers in clinical practice. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
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14 pages, 316 KiB  
Article
Clinical Variables Influence the Ability of miR-101, miR-150, and miR-21 to Predict Ventricular Remodeling after ST-Elevation Myocardial Infarction
by Liana Maries, Alexandra Ioana Moatar, Maria Sala-Cirtog, Laurentiu Sima, Andrei Anghel, Catalin Marian, Aimee Rodica Chis and Ioan-Ovidiu Sirbu
Biomedicines 2023, 11(10), 2738; https://doi.org/10.3390/biomedicines11102738 - 10 Oct 2023
Viewed by 756
Abstract
Left ventricle remodeling (LVR) after acute myocardial infarction (MI) leads to impairment of both systolic and diastolic function, a significant contributor to heart failure (HF). Despite extensive research in the field, predicting post-MI LVR and HF is still a challenge. Several circulant microRNAs [...] Read more.
Left ventricle remodeling (LVR) after acute myocardial infarction (MI) leads to impairment of both systolic and diastolic function, a significant contributor to heart failure (HF). Despite extensive research in the field, predicting post-MI LVR and HF is still a challenge. Several circulant microRNAs have been proposed as LVR predictors; however, their clinical value is controversial. Here, we used real-time quantitative PCR to quantify the plasma levels of hsa-miR-101, hsa-miR-150, and hsa-miR-21 on the first day of hospital admission of MI patients with ST-elevation (STEMI). We analyzed their correlation to the patient’s clinical and paraclinical variables and evaluated their ability to discriminate between post-MI LVR and non-LVR. We show that, despite being excellent MI discriminators, none of these microRNAs can distinguish between LVR and non-LVR patients. Furthermore, we found that diabetes mellitus (DM), Hb level, and the number of erythrocytes significantly influence all three plasma microRNA levels. This suggests that plasma microRNAs’ diagnostic and prognostic value in STEMI patients should be reevaluated and interpreted in the context of associated pathologies. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)

Review

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18 pages, 318 KiB  
Review
Exploring the Landscape of Anti-Inflammatory Trials: A Comprehensive Review of Strategies for Targeting Inflammation in Acute Myocardial Infraction
by Andreas Mitsis, Michaela Kyriakou, Stefanos Sokratous, Georgia Karmioti, Michail Drakomathioulakis, Michael Myrianthefs, Antonios Ziakas, Stergios Tzikas and George Kassimis
Biomedicines 2024, 12(3), 701; https://doi.org/10.3390/biomedicines12030701 - 21 Mar 2024
Viewed by 752
Abstract
The role of inflammation in the pathophysiology of acute myocardial infarction (AMI) is well established. In recognizing inflammation’s pivotal role in AMI, this manuscript systematically traces the historical studies spanning from early attempts to the present landscape. Several anti-inflammatory trials targeting inflammation in [...] Read more.
The role of inflammation in the pathophysiology of acute myocardial infarction (AMI) is well established. In recognizing inflammation’s pivotal role in AMI, this manuscript systematically traces the historical studies spanning from early attempts to the present landscape. Several anti-inflammatory trials targeting inflammation in post-AMI have been performed, and this review includes the key trials, as well as examines their designs, patient demographics, and primary outcomes. Efficacies and challenges are analyzed, thereby shedding light on the translational implications of trial outcomes. This article also discusses emerging trends, ongoing research, and potential future directions in the field. Practical applications and implications for clinical practice are considered by providing a holistic view of the evolving landscape of anti-inflammatory interventions in the context of AMI. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
22 pages, 2211 KiB  
Review
The Role of Pro-Opiomelanocortin Derivatives in the Development of Type 2 Diabetes-Associated Myocardial Infarction: Possible Links with Prediabetes
by Nompumelelo Anna-Cletta Gumede and Andile Khathi
Biomedicines 2024, 12(2), 314; https://doi.org/10.3390/biomedicines12020314 - 29 Jan 2024
Viewed by 905
Abstract
Myocardial infarction is a major contributor to CVD-related mortality. T2DM is a risk factor for MI. Stress activates the HPA axis, SNS, and endogenous OPS. These POMC derivatives increase the blood glucose and cardiovascular response by inhibiting the PI3K/AkT insulin signaling pathway and [...] Read more.
Myocardial infarction is a major contributor to CVD-related mortality. T2DM is a risk factor for MI. Stress activates the HPA axis, SNS, and endogenous OPS. These POMC derivatives increase the blood glucose and cardiovascular response by inhibiting the PI3K/AkT insulin signaling pathway and increasing cardiac contraction. Opioids regulate the effect of the HPA axis and SNS and they are cardioprotective. The chronic activation of the stress response may lead to insulin resistance, cardiac dysfunction, and MI. Stress and T2DM, therefore, increase the risk of MI. T2DM is preceded by prediabetes. Studies have shown that prediabetes is associated with an increased risk of MI because of inflammation, hyperlipidemia, endothelial dysfunction, and hypertension. The HPA axis is reported to be dysregulated in prediabetes. However, the SNS and the OPS have not been explored during prediabetes. The effect of prediabetes on POMC derivatives has yet to be fully explored and understood. The impact of stress and prediabetes on the cardiovascular response needs to be investigated. This study sought to review the potential impact of prediabetes on the POMC derivatives and pathways that could lead to MI. Full article
(This article belongs to the Special Issue Molecular Insights into Myocardial Infarction)
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