scholarly journals The Regulation Mechanisms and Clinical Application of MicroRNAs in Myocardial Infarction: A Review of the Recent 5 Years

2022 ◽  
Vol 8 ◽  
Author(s):  
Chan Wu ◽  
Binghong Liu ◽  
Ruiying Wang ◽  
Gang Li
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Structural Changes ◽  
Heart Tissue ◽  
Myocardial Remodeling ◽  
Irreversible Damage ◽  
Cardiovascular Pathology ◽  
The Past ◽  
Regulation Mechanisms ◽  
Non Coding Rnas

Myocardial infarction (MI) is the most frequent end-point of cardiovascular pathology, leading to higher mortality worldwide. Due to the particularity of the heart tissue, patients who experience ischemic infarction of the heart, still suffered irreversible damage to the heart even if the vascular reflow by treatment, and severe ones can lead to heart failure or even death. In recent years, several studies have shown that microRNAs (miRNAs), playing a regulatory role in damaged hearts, bring light for patients to alleviate MI. In this review, we summarized the effect of miRNAs on MI with some mechanisms, such as apoptosis, autophagy, proliferation, inflammatory; the regulation of miRNAs on cardiac structural changes after MI, including angiogenesis, myocardial remodeling, fibrosis; the application of miRNAs in stem cell therapy and clinical diagnosis; other non-coding RNAs related to miRNAs in MI during the past 5 years.

The role of non-coding RNA/microRNAs in cardiac disease

2018 ◽  
Author(s):  
Yolan J. Reckman ◽  
Yigal M. Pinto
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Hypertrophy ◽  
Cardiac Disease ◽  
Cardiac Development ◽  
Rna Transcripts ◽  
The Past ◽  
Non Coding Rna ◽  
Organ Systems ◽  
Non Coding Rnas

In the past two decades, our knowledge about non-coding DNA has increased tremendously. While non-coding DNA was initially discarded as ‘junk DNA’, we are now aware of the important and often crucial roles of RNA transcripts that do not translate into protein. Non-coding RNAs (ncRNAs) play important functions in normal cellular homeostasis and also in many diseases across all organ systems. Among the different ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have been studied the most. In this chapter we discuss the role of miRNAs and lncRNAs in cardiac disease. We present examples of miRNAs with fundamental roles in cardiac development (miR-1), hypertrophy (myomiRs, miR-199, miR-1/133), fibrosis (miR-29, miR-21), myocardial infarction (miR-15, miR17~92), and arrhythmias/conduction (miR-1). We provide examples of lncRNAs related to cardiac hypertrophy (MHRT, CHRF), myocardial infarction (ANRIL, MIAT), and arrhythmias (KCNQ1OT1). We also discuss miRNAs and lncRNAs as potential therapeutic targets or biomarkers in cardiac disease.

scholarly journals Intracoronary delivery of recombinant TIMP-3 after myocardial infarction: effects on myocardial remodeling and function

2017 ◽  
Vol 313 (4) ◽  
pp. H690-H699 ◽  
Author(s):  
Shayne C. Barlow ◽  
Heather Doviak ◽  
Julia Jacobs ◽  
Lisa A. Freeburg ◽  
Paige E. Perreault ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Matrix Metalloproteinase ◽  
Reperfusion Injury ◽  
Targeted Delivery ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Remodeling ◽  
Myocardial Ischemia And Reperfusion ◽  
End Diastolic Volume

Ischemia-reperfusion (IR) and myocardial infarction (MI) cause adverse left ventricular (LV) remodeling and heart failure and are facilitated by an imbalance in matrix metalloproteinase (MMP) activation and the endogenous tissue inhibitors of metalloproteinase (TIMPs). We have identified that myocardial injections of recombinant TIMP-3 (rTIMP-3; human full length) can interrupt post-MI remodeling. However, whether and to what degree intracoronary delivery of rTIMP-3 post-IR is feasible and effective remained to be established. Pigs (25 kg) underwent coronary catheterization and balloon occlusion of the left anterior descending coronary artery (LAD) for 90 min whereby at the final 4 min, rTIMP-3 (30 mg, n = 9) or saline was infused in the distal LAD. LV echocardiography was performed at 3–28 days post-IR, and LV ejection fraction (EF) and LV end-diastolic volume were measured. LV EF fell and LV end-diastolic volume increased from baseline (pre-IR) values (66 ± 1% and 40 ± 1 ml, respectively, means ± standard deviation) in both groups; however, the extent of LV dilation was reduced in the rTIMP-3 group by 40% at 28 days post-IR ( P < 0.05) and the fall in LV EF was attenuated. Despite equivalent plasma troponin levels (14 ± 3 ng/ml), computed MI size at 28 days was reduced by over 45% in the rTIMP-3 group ( P < 0.05), indicating that rTIMP-3 treatment abrogated MI expansion post-IR. Plasma NH2-terminal pro-brain natriuretic peptide levels, an index of heart failure progression, were reduced by 25% in the rTIMP-3 group compared with MI saline values ( P < 0.05). Although the imbalance between MMPs and TIMPs has been recognized as a contributory factor for post-MI remodeling, therapeutic strategies targeting this imbalance have not been forthcoming. This study is the first to demonstrate that a relevant delivery approach (intracoronary) using rTIMP can alter the course of post-MI remodeling. NEW & NOTEWORTHY Myocardial ischemia and reperfusion injury remain significant causes of morbidity and mortality whereby alterations in the balance between matrix metalloproteinase and tissue inhibitor of metalloproteinase have been identified as contributory biological mechanisms. This novel translational study advances the concept of targeted delivery of recombinant proteins to modify adverse myocardial remodeling in ischemia-reperfusion injury.

scholarly journals Microarray Expression Profile of Circular RNAs in Heart Tissue of Mice with Myocardial Infarction-Induced Heart Failure

2016 ◽  
Vol 39 (1) ◽  
pp. 205-216 ◽  
Author(s):  
Hong-Jin Wu ◽  
Cheng-Ying Zhang ◽  
Sai Zhang ◽  
Min Chang ◽  
Hong-Yun Wang
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Potential Role ◽  
Expression Patterns ◽  
Heart Tissue ◽  
Circular Rnas ◽  
Global Changes ◽  
Microarray Expression ◽  
Microarray Expression Profile

Background/Aims: Myocardial infarction (MI) is a serious complication of atherosclerosis associated with increasing mortality attributable to heart failure. This study is aimed to assess the global changes in and characteristics of the transcriptome of circular RNAs (circRNAs) in heart tissue during MI induced heart failure (HF). Methods: Using a post-myocardial infarction (MI) model of HF in mice, we applied microarray assay to examine the transcriptome of circRNAs deregulated in the heart during HF. We confirmed the changes in circRNAs by quantitative PCR. Results: We revealed and confirmed a number of circRNAs that were deregulated during HF, which suggests a potential role of circRNAs in HF. Conclusions: The distinct expression patterns of circulatory circRNAs during HF indicate that circRNAs may actively respond to stress and thus serve as biomarkers of HF diagnosis and treatment.

scholarly journals A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Leonardo Schirone ◽  
Maurizio Forte ◽  
Silvia Palmerio ◽  
Derek Yee ◽  
Cristina Nocella ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
Volume Overload ◽  
Cardiac Complications ◽  
Compensatory Mechanism ◽  
Myocardial Remodeling ◽  
Heart Failure Progression ◽  
Complex Signaling

Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.

scholarly journals Beta-blockers, and real clinical practice in Russia: the gap between the understanding of the doses of beta-blockers and subsequent prognosis in patients with cardiovascular disease

2017 ◽  
Vol 14 (3) ◽  
pp. 36-41
Author(s):  
I V Fomin ◽  
D S Polyakov
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Chronic Heart Failure ◽  
Beta Blockers ◽  
Previous History ◽  
Clinical Manifestations ◽  
Population Level ◽  
Cardiovascular Pathology ◽  
History Of

Presents an analysis of the reception beta-blockers in three epidemiological studies sections of the EPOKhA. Respondents in each slice (2002, 2007, 2017) were stratified into 5 subgroups: only suffering from hypertension - AH (subgroup AH), patients with stable angina pectoris, but in history and clinically has no evidence of acute myocardial infarction (AMI) and chronic heart failure (subgroup of coronary heart disease); after myocardial infarction, but do not have clinical manifestations of chronic heart failure (subgroup myocardial infarction); patients with acute myocardial infarction formed for any reason, but with no previous history of AMI (subgroup chronic heart failure), and patients with clinical manifestations of chronic heart failure after suffering AMI in anamnesis (subgroup myocardial infarction + chronic heart failure). During 15 years in the Russian Federation the frequency of administration of beta-blockers increased from 20% in the section of cardiovascular pathology to 30%. The most sensitive to the use of beta-blockers were patients with a history of AMI and chronic heart failure. Prolonged beta-blockers have been used at the population level only in 2007, but the frequency with any cardiovascular pathology does not exceed the 50% threshold, and the achievement of goals (control heart rate) does not exceed 10% of the level at any pathology. This dependence is associated with low-dose beta-blockers. In any case, the dose of beta-blockers did not exceed 50% of recommended that can be a separate cause of cardiovascular mortality at the population level in Russia.

Abstract 383: Heart-Kidney: Myocardial Infarction Mediates Renal Fibrosis and Activates Renal Molecular Remodeling in the Absence of Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Fernando L Martin ◽  
Brenda K Huntley ◽  
Gerald E Harders ◽  
Sharon M Sandberg ◽  
Horng H Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Renal Function ◽  
Microarray Analysis ◽  
Structural Changes ◽  
Cell Communication ◽  
Kidney Cortex ◽  
Water Excretion ◽  
Mild Reduction ◽  
Poor Outcomes

Background : Studies in human myocardial infarction (MI) suggest that even in the absence of heart failure (HF) alterations in renal function may occur and contribute to poor outcomes. After MI a decline in renal function may be seen acutely by mechanisms which are unclear. The long term consequences of MI upon renal function and structure remain poorly defined. We hypothesized that even without pre-existing renal disease, renal functional and structural changes would be present following MI. Methods : Cardiorenal function and structure were assessed in Wistar rats, Sham (S; n=10) and MI groups (n=9) 3 weeks after MI. GFR was determined by inulin clearance. Blood was obtained for PRA and aldosterone. Hearts and kidneys were harvested for histological analysis. Cardiac function was assessed by echo. Genome-wide microarray analysis was performed on kidney cortex (KC) and medulla (KM) (Affymetrix GeneChip® Rat Genome 230 2.0). Results : EF decreased after MI (S:62.8±2.3, MI:42.8±6.5 %, p<0.01) and LVEDd increased (p<0.005) PRA and aldosterone activation were absent. Blood pressure (BP) was not different between groups. There was no HF as sodium and water excretion was maintained. GFR tended to decrease (S:2.9±0.3, MI:2.4±0.2 ml/min, NS). Picrosirius Red staining for collagen in the KC and KM after MI showed greater fibrosis especially in the RM (KC S:1.1±0.2, MI:3.5±0.6 %, p<0.001 and KM S:1±0.2, MI:18.8±6 %, p<0.005). Microarray analysis revealed that 303 genes significantly changed in KM and 407 genes in the KC after MI (1.5 fold, P<0.05). Gene dysregulation was related to cell proliferation, metabolic processes and cell communication (Z value>2). Conclusion : We conclude that experimental MI results in renal structural remodeling characterized by renal cortical and medullary fibrosis with a mild reduction in GFR and extensive modulation of molecular pathways related to renal growth and metabolism. This investigation provides evidence for a heart-kidney connection after MI by mechanisms which remain to be defined. We also conclude that therapies for MI targeting the heart also should be evaluated for properties of renoprotection.

Ischaemia, hibernation, and viability

2021 ◽  
pp. 53-56
Author(s):  
Roberto Ferrari
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Scientific Community ◽  
Structural Changes ◽  
Coronary Bypass ◽  
Left Ventricular ◽  
Hibernating Myocardium ◽  
Irreversible Damage ◽  
Artery Disease

It was dogma for many years that if myocardial ischaemia persists for more than 30 minutes, necrosis will develop, resulting in myocardial infarction. The unavoidable extrapolation of that dogma suggested that chronic ischaemia, in reality, cannot exist, as it will inevitably evolve into structural changes (i.e. irreversible damage). These tenets were overturned in the early 1980s when Rahimtoola reviewed the results of coronary bypass surgery trials and identified patients with coronary artery disease and chronic left ventricular dysfunction persisting for months and even years that improved after revascularization. The rapid amelioration of myocardial function obtained by revascularization ruled out the hypothesis that the reduced function was due to histological modification of the myocardium and left the entire scientific community with the dilemma to explain and recognize hibernating myocardium.

scholarly journals INFLUENCE OF COMPLEX TREATMENT WITH MAGNESIUM AND POTASSIUM SALTS OF GLUCONIC ACID, EPLERENONE AND RIVAROXABAN ON DYNAMICS OF INDICATORS OF ISCHEMIA AND MYOCARDIAL REMODELING IN PATIENTS WITH CHRONIC HEART FAILURE AFTER MYOCARDIAL INFARCTION

2021 ◽  
Vol 74 (9) ◽  
pp. 2087-2093
Author(s):  
Igor P. Vakaliuk ◽  
Nataliia V. Savchuk ◽  
Roksolana V. Nesterak ◽  
Haliia B. Kulynych ◽  
Ruslana S. Hryhoryshyn
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Gluconic Acid ◽  
Treatment Effectiveness ◽  
Reverse Remodeling ◽  
Myocardial Remodeling ◽  
Complex Treatment ◽  
Potassium Salts ◽  
Clinical Cardiology ◽  
Complex Therapy

The aim: To increase the treatment effectiveness of CHF patients after MI with stenting by using magnesium and potassium salts of gluconic acid, eplerenone, and rivaroxaban in complex therapy. Materials and methods: The research was performed at the premises of Ivano-Frankivsk Regional Clinical Cardiology Centre, Ukraine. 84 patients with CHF after past MI were examined. Results and conclusions: A more pronounced anti-ischemic effect has been linked to the use of combination therapy with rivaroxaban on the background of basic therapy (BT) in patients with CHF after MI, compared with the use of magnesium and potassium salts of gluconic acid or eplerenone. The use of eplerenone in the complex treatment of these patients on the background of BT has been proven to provide a pronounced reverse remodeling of the left myocardium in the postinfarction period.

scholarly journals Incidence of myocardial infarction, heart failure, and cardiovascular mortality in patients with peripheral artery disease: nationwide trends between 1997 and 2016

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
S Kamil ◽  
T S G Sehested ◽  
K Houlind ◽  
J F Lassen ◽  
G Gislason ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Peripheral Artery Disease ◽  
Cumulative Incidence ◽  
Incidence Rates ◽  
Peripheral Artery ◽  
The Past ◽  
Artery Disease ◽  
First Time ◽  
Time Diagnosis

Abstract Background Over the past decades there has been a shift in cardiovascular (CV) risk factors with improved outcomes. Updated trends in incidence of myocardial infarction (MI) and heart failure (HF) in peripheral artery disease (PAD) are warranted. Purpose We aimed to investigate trends in the incidence of MI, HF, and CV mortality in PAD patients during the past two decades. Methods Nationwide registers were used to identify all patients aged ≥18 years, with first-time diagnosis of PAD between 1997 and 2016. Age-standardized incidence rates per 1,000 person-years (IR) were calculated to estimate trends of MI, HF, and CV mortality. Furthermore, risk of MI, HF, and CV mortality was estimated by 1-year cumulative-incidence with death as competing risk. Results A total of 136,746 patients with first-time diagnosis of PAD were included. Mean age was 70.01 [IQR 61–77 years], and 53.05% of the identified patients were male. The 1-year cumulative-incidence of MI in patients with PAD were 1.88% for year 1997–2000, 2.12% for year 2001–2005, 1.59% for year 2006–2010, and 1.32% for year 2011–2016, respectively. The 1-year cumulative-incidence of HF in patients with PAD were 1.71%, 1.48%, 1.25%, and 1.11% for the 1997–2000, 2001–2005, 2006–2010, and 2011–2016 year-groups, respectively. Furthermore the 1-year cumulative-incidence of CV mortality in patients with PAD were 12.0%, 9.41%, 8.75%, and 7.80% for the 1997–2000, 2001–2005, 2006–2010, and 2011–2016 year-groups, respectively. Likewise, the age-standardized incidence rates pr. 1,000 person-years showed increasing trends of MI up until 2002 with an estimated annual percent change (APC) of +0.6 (95% CI 3.3–16.1, p-value 0.2). After year 2002 the IR decreased significantly with an estimated APC of −5.0 (95% CI 3.7–6.3, p&lt;0.0001). The age-standardized IR for HF decreased with an estimated APC of −3.3 (95% CI 2.0–4.6, p&lt;0.0001), and similarly for CV death decreased by −3.5 (95% CI 3.0–4.0, p&lt;0.0001). Conclusion The incidence of MI and HF in patients with PAD has significantly decreased over time together with a subsequent decline in CV mortality. This may suggest that the improvements in preventive strategies aimed at reducing CV risk are effective and contributes to lower incidence of MI and HF and thereby improved mortality rates in the past two decades. FUNDunding Acknowledgement Type of funding sources: None.

Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure

2003 ◽  
Vol 285 (1) ◽  
pp. H442-H448 ◽  
Author(s):  
David Sheikh-Hamad ◽  
Roger Bick ◽  
Gang-Yi Wu ◽  
Birgitte Mønster Christensen ◽  
Peter Razeghi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Structural Changes ◽  
Cardiac Tissue ◽  
Heart Tissue ◽  
Left Ventricular ◽  
Calcium Currents ◽  
Human Heart Failure ◽  
Rat Cardiomyocytes ◽  
Failing Heart ◽  
Mechanical Unloading

Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Because the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in the heart, we reasoned that STC1 might play a role in the adaptive-maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using a left ventricular assist device (LVAD), and we compared the results with those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes and arterial walls of failing hearts pre-LVAD and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole cell patch-clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of transmembrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart.

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