scholarly journals Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology

2021 ◽  
Vol 8 ◽  
Author(s):  
Wei Wang ◽  
Hao Zheng
Keyword(s):  
Myocardial Infarction ◽  
Protective Role ◽  
Severe Form ◽  
Pathological Process ◽  
Cardiomyocyte Hypertrophy ◽  
Therapeutic Effects ◽  
Myocardial Apoptosis ◽  
Micro Rnas ◽  
Future Direction

Cardiovascular diseases have been regarded as the leading cause of death around the world, with myocardial infarction (MI) being the most severe form. MI leads to myocardial apoptosis, cardiomyocyte fibrosis, and cardiomyocyte hypertrophy, ultimately leading to heart failure, and death. Micro RNAs (miRNAs) participate in the genesis and progression of myocardial pathology after MI by playing an important regulatory role. This review aims to summarize all available knowledge on the role of miRNAs in the myocardial pathological process after MI to uncover potential major target pathways. In addition, the main therapeutic methods and their latest progress are also reviewed. miRNAs can regulate the main signaling pathways as well as pathological processes. Thus, they have the potential to induce therapeutic effects. Hence, the combination of miRNAs with recently developed exosome nanocomplexes may represent the future direction of therapeutics.

scholarly journals Novel Therapeutic Effects of Pterosin B on Ang II-Induced Cardiomyocyte Hypertrophy

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5279
Author(s):  
Chang Youn Lee ◽  
Han Ki Park ◽  
Bok-Sim Lee ◽  
Seongtae Jeong ◽  
Sung-Ae Hyun ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Protective Role ◽  
Cardiomyocyte Hypertrophy ◽  
Therapeutic Effects ◽  
Ang Ii ◽  
Pathological Cardiac Hypertrophy ◽  
Glycation End Products ◽  
Abnormal Increase

Pathological cardiac hypertrophy is characterized by an abnormal increase in cardiac muscle mass in the left ventricle, resulting in cardiac dysfunction. Although various therapeutic approaches are being continuously developed for heart failure, several studies have suggested natural compounds as novel potential strategies. Considering relevant compounds, we investigated a new role for Pterosin B for which the potential life-affecting biological and therapeutic effects on cardiomyocyte hypertrophy are not fully known. Thus, we investigated whether Pterosin B can regulate cardiomyocyte hypertrophy induced by angiotensin II (Ang II) using H9c2 cells. The antihypertrophic effect of Pterosin B was evaluated, and the results showed that it reduced hypertrophy-related gene expression, cell size, and protein synthesis. In addition, upon Ang II stimulation, Pterosin B attenuated the activation and expression of major receptors, Ang II type 1 receptor and a receptor for advanced glycation end products, by inhibiting the phosphorylation of PKC-ERK-NF-κB pathway signaling molecules. In addition, Pterosin B showed the ability to reduce excessive intracellular reactive oxygen species, critical mediators for cardiac hypertrophy upon Ang II exposure, by regulating the expression levels of NAD(P)H oxidase 2/4. Our results demonstrate the protective role of Pterosin B in cardiomyocyte hypertrophy, suggesting it is a potential therapeutic candidate.

Molecular understanding of the protective role of natural products on isoproterenol-induced myocardial infarction: A review

2017 ◽  
Vol 94 ◽  
pp. 1145-1166 ◽  
Author(s):  
Zheng Wei Wong ◽  
Punniyakoti Veeraveedu Thanikachalam ◽  
Srinivasan Ramamurthy
Keyword(s):  
Myocardial Infarction ◽  
Natural Products ◽  
Protective Role

Abstract 507: Activation of the Classically Pro-Apoptotic Death Receptor 5 Promotes Physiological Hypertrophy and Cardiomyocyte Survival

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Toby Thomas ◽  
Miles Tanner ◽  
Laurel Grisanti
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cardiac Fibrosis ◽  
Death Receptor ◽  
Protective Role ◽  
Cardiomyocyte Hypertrophy ◽  
Death Receptor 5 ◽  
Tnf Α ◽  
Cardiomyocyte Survival

Heart failure is hallmarked by a combination of cardiomyocyte hypertrophy and death. Apoptosis, one of the primary mechanisms of cell death, occurs through finely tuned extrinsic or intrinsic pathways. Of the mediators involved in extrinsic apoptotic signaling, some have been extensively studied, such as tumor necrosis factor ((TNF)-α), while others have been relatively untouched. One such receptor is Death Receptor 5 (DR5) which, along with its ligand TNF-Related Apoptosis Inducing Ligand (TRAIL), have recently been implicated as a biomarker in determining the progression and outcome in patients following multiple heart failure etiologies, suggesting a novel role of DR5 signaling in the heart. These studies suggest a potentially protective role for DR5 in the heart; however, the function of TRAIL/DR5 in the heart has been virtually unstudied. Our goal was to explore the role of TRAIL/DR5 in cardiomyocyte hypertrophy and survival with the hypothesis that DR5 promotes cardiomyocyte survival and growth through non-canonical mechanisms. Mice treated with the DR5 agonist bioymifi or a DR5 agonist antibody, MD5-1, were absent of cell death, while an increase in hypertrophy was observed without a decline in cardiac function. In isolated cardiomyocytes, this pro-hypertrophic phenotype was determined to operate through MMP-dependent cleavage of HB-EGFR, leading to transactivation of EGFR and ERK1/2 signaling. To determine the role of DR5 in heart failure, a chronic catecholamine administration model was used and DR5 activation was found to decrease cardiomyocyte death and cardiac fibrosis. ERK1/2, a well characterized pro-survival, pro-hypertrophic kinase is activated in the heart with DR5 agonist administration and may represent the mechanistic link through which DR5 is imparting cardioprotection. In summary, DR5 activation promotes cardiomyocyte hypertrophy and survival and prevents cardiac fibrosis via a non-canonical MMP-EGFR-ERK1/2 pathway. Taken together, these studies identify a previously undetermined role for DR5 in the heart and identify novel therapeutic target for the treatment of heart failure.

Role of adiponectin receptors in endothelin-induced cellular hypertrophy in cultured cardiomyocytes and their expression in infarcted heart

2006 ◽  
Vol 290 (6) ◽  
pp. H2409-H2416 ◽  
Author(s):  
Daisuke Fujioka ◽  
Ken-ichi Kawabata ◽  
Yukio Saito ◽  
Tsuyoshi Kobayashi ◽  
Takamitsu Nakamura ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Full Length ◽  
Cardiomyocyte Hypertrophy ◽  
Leucine Incorporation ◽  
Adiponectin Receptors ◽  
Cellular Hypertrophy ◽  
Globular Adiponectin ◽  
Interfering Rna ◽  
Cultured Cardiomyocytes

Adiponectin, an adipocyte-derived protein, has cardioprotective actions. We elucidated the role of the adiponectin receptors AdipoR1 and AdipoR2 in the effects of adiponectin on endothelin-1 (ET-1)-induced hypertrophy in cultured cardiomyocytes, and we examined the expression of adiponectin receptors in normal and infarcted mouse hearts. Recombinant full-length adiponectin suppressed the ET-1-induced increase in cell surface area and [3H]leucine incorporation into cultured cardiomyocytes compared with cells treated with ET-1 alone. Transfection of small interfering RNA (siRNA) specific for AdipoR1 or AdipoR2 reversed the suppressive effects of adiponectin on ET-1-induced cellular hypertrophy in cultured cardiomyocytes. Adiponectin induced phosphorylation of AMP-activated protein kinase (AMPK) and inhibited ET-1-induced ERK1/2 phosphorylation, which were also reversible by transfection of siRNA for AdipoR1 or AdipoR2 in cultured cardiomyocytes. Transfection of siRNA for α2-catalytic subunits of AMPK reduced the inhibitory effects of adiponectin on ET-1-induced cellular hypertrophy and ERK1/2 phosphorylation. Effects of globular adiponectin were similar to those of full-length adiponectin, and siRNA for AdipoR1 reversed the actions of globular adiponectin. Compared with normal left ventricle, expression levels of AdipoR1 mRNA and protein were decreased in the remote, as well as the infarcted, area after myocardial infarction in mouse hearts. In conclusion, AdipoR1 and AdipoR2 mediate the suppressive effects of full-length and globular adiponectin on ET-1-induced hypertrophy in cultured cardiomyocytes, and AMPK is involved in signal transduction through these receptors. AdipoR1 and AdipoR2 might play a role in the pathogenesis of ET-1-related cardiomyocyte hypertrophy after myocardial infarction.

Protective role of DDAH2 (rs805304) gene polymorphism in patients with myocardial infarction

2014 ◽  
Vol 97 (3) ◽  
pp. 393-398 ◽  
Author(s):  
Nonanzit Pérez-Hernández ◽  
Gilberto Vargas-Alarcón ◽  
Rocio Arellano-Zapoteco ◽  
Nancy Martínez-Rodríguez ◽  
José Manuel Fragoso ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Gene Polymorphism ◽  
Protective Role

scholarly journals The Role of Mitochondria in Pyroptosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Qian Li ◽  
Nengxian Shi ◽  
Chen Cai ◽  
Mingming Zhang ◽  
Jing He ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Pathological Process ◽  
Mitochondrial Outer Membrane ◽  
Therapeutic Effects ◽  
Mitochondrial Outer Membrane Permeabilization ◽  
Regulated Cell Death ◽  
Clinical Benefits ◽  
Regulate Cell Death

Pyroptosis is a recently discovered aspartic aspart-specific cysteine protease (Caspase-1/4/5/11) dependent mode of gene-regulated cell death cell death, which is represented by the rupture of cell membrane perforations and the production of proinflammatory mediaters like interleukin-18(IL-18) and interleukin-1β (IL-1β). Mitochondria also play an important role in apoptotic cell death. When it comes to apoptosis of mitochondrion, mitochondrial outer membrane permeabilization (MOMP) is commonly known to cause cell death. As a downstream pathological process of apoptotic signaling, MOMP participates in the leakage of cytochrome-c from mitochondrion to the cytosol and subsequently activate caspase proteases. Hence, targeting MOMP for the sake of manipulating cell death presents potential therapeutic effects among various types of diseases, such as autoimmune disorders, neurodegenerative diseases, and cancer. In this review, we highlights the roles and significance of mitochondria in pyroptosis to provide unexplored strategies that target the mitochondria to regulate cell death for clinical benefits.

scholarly journals Explore the Protective Role of Obesity in the Progression of Myocardial Infarction

2021 ◽  
Vol 8 ◽  
Author(s):  
Siyuan Zhao ◽  
Rongyuan Cao ◽  
Shuhua Zhang ◽  
Yan Kang
Keyword(s):  
Myocardial Infarction ◽  
Blood Pressure ◽  
Regulatory Networks ◽  
Large Scale ◽  
Enrichment Analysis ◽  
Protective Role ◽  
Gene Set Enrichment Analysis ◽  
Shortest Path Analysis ◽  
Acute Mi

Obesity has been shown as a risk factor to increase the incidence of myocardial infarction (MI). However, obesity has also been linked to the decreased mortality of acute MI with unknown mechanisms. Here, we firstly used large-scale literature data mining to identify obesity downstream targets and MI upstream regulators with polarity, based on which an obesity-MI regulatory network was constructed. Then, a gene set enrichment analysis was conducted to explore the functional profile of the genes involved in the obesity-MI regulatory networks. After that, a mega-analysis using MI RNA expression datasets was conducted to test the expression of obesity-specific genes in MI patients, followed by a shortest-path analysis to explore any potential gene-MI association. Our results suggested that obesity could inhibit 11 MI promoters, including NPPB, NPPA, IRS1, SMAD3, MIR155, ADRB1, AVP, MAPK14, MC3R, ROCK1, and COL3A1, which were mainly involved in blood pressure-related pathways. Our study suggested that obesity could influence MI progression by driving multiple genes associated with blood pressure regulation. Moreover, PTH could be a novel obesity driven gene associated with the pathogenesis of MI, which needs further validation.

scholarly journals New Insights on the Role of pentraxin-3 in Allergic Asthma

2021 ◽  
Vol 2 ◽  
Author(s):  
Latifa Koussih ◽  
Samira Atoui ◽  
Omar Tliba ◽  
Abdelilah S. Gounni
Keyword(s):  
Immune Response ◽  
Allergic Asthma ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Protective Role ◽  
Severe Form ◽  
Innate Immune ◽  
Pentraxin 3 ◽  
Complement Components

Pentraxins are soluble pattern recognition receptors that play a major role in regulating innate immune responses. Through their interaction with complement components, Fcγ receptors, and different microbial moieties, Pentraxins cause an amplification of the inflammatory response. Pentraxin-3 is of particular interest since it was identified as a biomarker for several immune-pathological diseases. In allergic asthma, pentraxin-3 is produced by immune and structural cells and is up-regulated by pro-asthmatic cytokines such as TNFα and IL-1β. Strikingly, some recent experimental evidence demonstrated a protective role of pentraxin-3 in chronic airway inflammatory diseases such as allergic asthma. Indeed, reduced pentraxin-3 levels have been associated with neutrophilic inflammation, Th17 immune response, insensitivity to standard therapeutics and a severe form of the disease. In this review, we will summarize the current knowledge of the role of pentraxin-3 in innate immune response and discuss the protective role of pentraxin-3 in allergic asthma.

scholarly journals Haematopoietic and Cardiac GPR55 Synchronize Post-myocardial Infarction Remodelling

2021 ◽  
Author(s):  
Sarah-Lena Puhl ◽  
Michael Hilby ◽  
Michael Kohlhaas ◽  
Linus M. Keidel ◽  
Yvonne Jansen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cannabinoid Receptors ◽  
Sarcomere Length ◽  
Myeloid Cell ◽  
Cardiomyocyte Hypertrophy ◽  
Chemokine Production ◽  
Inflammatory Phenotype ◽  
Infarct Expansion ◽  
Lv Volume

Abstract Background and purpose: While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Methods and results: Global GPR55-/- and wildtype (WT) mice were basally characterized or assigned to 1, 3 or 28 days permanent MI and subsequently analysed via pro-inflammatory and pro-hypertrophic parameters. GPR55-/- deficiency was basally associated with bradycardia, increased diastolic LV volume and sarcomere length and a subtle inflammatory phenotype. While infarct size and myeloid cell infiltration were unaffected by GPR55 depletion, acute cardiac chemokine production was prolonged post-MI. Concurrently, GPR55-/- hearts exhibited a premature expansion of pro-reparative and phagocytic macrophages paralleled by early up regulation of extracellular matrix (ECM) factors 3 days post-MI, which could be mimicked by sole haematopoietic GPR55 depletion. Moreover, global GPR55 deficiency mitigated MI-induced foetal gene re-programming and cardiomyocyte hypertrophy, culminating in aggravated LV dilatation and infarct expansion. Conclusions: GPR55 regulates cardiac homeostasis and ischaemia responses by maintaining adequate LV filling and modulating three crucial processes post-MI: wound healing kinetics, cardiomyocyte hypertrophy and maladaptive remodelling.

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