scholarly journals Modes of Myocardial Cell Injury and Cell Death in Ischemic Heart Disease

Circulation ◽  
1998 ◽  
Vol 98 (14) ◽  
pp. 1355-1357 ◽  
Author(s):  
L. Maximilian Buja ◽  
Mark L. Entman
Keyword(s):  
Cell Death ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Ischemic Heart ◽  
Myocardial Cell Injury

scholarly journals The Current Dilemma and Breakthrough of Stem Cell Therapy in Ischemic Heart Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Chuanbin Liu ◽  
Dong Han ◽  
Ping Liang ◽  
Yang Li ◽  
Feng Cao
Keyword(s):  
Stem Cell ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cell Fate ◽  
Clinical Studies ◽  
Myocardial Cell ◽  
Ischemic Heart ◽  
Cell Based Therapy ◽  
Cell Engraftment ◽  
Functional Mechanisms

Ischemic heart disease (IHD) is the leading cause of mortality worldwide. Stem cell transplantation has become a promising approach for the treatment of IHD in recent decades. It is generally recognized that preclinical cell-based therapy is effective and have yielded encouraging results, which involves preventing or reducing myocardial cell death, inhibiting scar formation, promoting angiogenesis, and improving cardiac function. However, clinical studies have not yet achieved a desired outcome, even multiple clinical studies showing paradoxical results. Besides, many fundamental puzzles remain to be resolved, for example, what is the optimal delivery timing and approach? Additionally, limited cell engraftment and survival, challenging cell fate monitoring, and not fully understood functional mechanisms are defined hurdles to clinical translation. Here we review some of the current dilemmas in stem cell-based therapy for IHD, along with our efforts and opinions on these key issues.

scholarly journals Botanical Flavonoids on Coronary Heart Disease

2011 ◽  
Vol 39 (04) ◽  
pp. 661-671 ◽  
Author(s):  
Chong-Zhi Wang ◽  
Sangeeta R. Mehendale ◽  
Tyler Calway ◽  
Chun-Su Yuan
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Herbal Medicines ◽  
Grape Seed ◽  
Ischemic Heart ◽  
Care Costs

Ischemic heart disease (IHD) is one of the leading causes of death in Western countries. Prevention rather than treatment of heart disease can significantly improve patients' quality of life and reduce health care costs. Flavonoids are widely distributed in vegetables, fruits and herbal medicines. Regularly consuming botanicals, especially those containing flavonoids, has been associated with a reduction in cardiovascualar disease; thus, it is important to investigate how flavonoids improve cardiac resistance to heart disease and their related mechanisms of action. It has been shown that cardiomyocyte injury and death can result from ischemia-reperfusion, which is pathognomonic of ischemic heart disease. Massive reactive oxygen species (ROS) release at the onset of reperfusion produces cell injury and death. "Programming" the heart to either generate less ROS or to increase strategic ROS removal could reduce reperfusion response. Additionally, profuse nitric oxide (NO) release at reperfusion could be protective in "preconditioning" models. Botanical flavonoids induce preconditioning of the heart, thereby protecting against ischemia-reperfusion injury. In this article, we will discuss two herbs containing potent flavonoids, Scutellaria baicalensis and grape seed proanthocyanidin, which can potentially offer cardiac protection against ischemic heart disease.

scholarly journals ДІАГНОСТИКА ХРОНІЧНОЇ СЕРЦЕВОЇ НЕДОСТАТНОСТІ СОБАК – ІСНУЮЧІ МЕТОДИ ТА ПОДАЛЬШІ ПЕРСПЕКТИВИ

2016 ◽  
Vol 18 (3(71)) ◽  
pp. 130-133
Author(s):  
R. Trofimjak ◽  
L. Slivinska
Keyword(s):  
Molecular Weight ◽  
Heart Disease ◽  
Cardiac Troponin ◽  
Cell Injury ◽  
Troponin I ◽  
Myocardial Cell ◽  
Response To Therapy ◽  
Cardiac Biomarkers ◽  
Myocardial Cell Injury ◽  
Cardiac Troponins

The article analyzes the current scientific work related to the study of processes of chronic heart failure (CHF), and the use of biomarkers in the diagnosis of heart disease in dogs. Thoracic radiography, electrocardiography, and echocardiography are used to diagnose heart disease in dogs but despite the use of non–invasive methods, there is uncertainty about the severity of the disease and prognosis for each patient individually. In veterinary practice for the diagnosis of myocardial lesions in animals are clinically valuable, highly sensitive and simple to use cardiac biomarkers. A biomarker is typically a substance in the blood that can be objectively measured and indicates a biologic or pathologic process or response to therapy.1 There are scores of cardiac biomarkers,but this article will focus on the 2 most clinically useful ones in the dog and cat:cardiac troponin I (cTnI) and N–terminal pro–B–type natriuretic peptide (NT–proBNP). The cardiac troponins I, T, and C (cTnI, cTnT, and cTnC) are thin filament–associated regulatory proteins of the heart muscle. Cardiac troponin I («I» for inhibition) is uniquely expressed in the myocardium and is a potent inhibitor of the process of actin–myosin cross–bridge formation. The molecular weight is 24.000 D. Cardiac troponin T («T» for tropomyosin binding) has a molecular weight of 37.000 D and binds the troponin complex to tropomyosin. Cardiac troponin C («C» for calcium) binds to calcium and starts, therefore, the crossbridge cycle. As with cTnI, approximately 95% of cTnT in man and dogs is myofibril bound and about 5% is cytosolically dissolved. Mechanisms for an elevation in circulating cardiac troponins include an increase of myocyte membrane permeability (initial release of the cytosolic troponin pool) or cell necrosis (release of myofibrilbound troponins). Four to six hours after acute myocardial cell injury, the cardiac troponin concentration in blood increases in a biphasic pattern. Plasma half–life of cardiac troponins is approximately two hours, and elimination mainly occurs via the reticuloendothelial system (cTnI and cTnT) and renal loss (cTnT). Cardiac troponins are phylogenetically highly preserved proteins with a more than 95% total structural agreement between mammals. Therefore, established human serologic tests for troponin analysis may be used reliably in pets as well. Myocardial cell injury, manifested anatomically as inflammation (endomyocarditis, myocarditis, perimyocarditis), acute degeneration, apoptosis, or necrosis or hemodynamically as transient or permanent cardiac contractile dysfunction, is a frequent consequence of physical myocardial trauma (cardiac contusion), cardiomyopathy, metabolic or toxic myocardial damage (anthracyclines, catecholamines, bacterial endotoxins, tumor necrosis factor), myocardial ischemia or infarction. However, early diagnosis of myocardial injury may be important from a therapeutic and prognostic perspective. 

Maitotoxin-induced myocardial cell injury: Calcium accumulation followed by ATP depletion precedes cell death

1990 ◽  
Vol 102 (1) ◽  
pp. 164-173 ◽  
Author(s):  
Giovanni Santostasi ◽  
R.Krishnan Kutty ◽  
Antonio L. Bartorelli ◽  
Takeshi Yasumoto ◽  
Gopal Krishna
Keyword(s):  
Cell Death ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Atp Depletion ◽  
Calcium Accumulation ◽  
Myocardial Cell Injury

Abstract 467: ATF6B and ATF6A Play Complimentary Roles in Mediating Adaptive and Maladaptive Signaling in Cardiac Myocytes

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Shivsmriti Koul ◽  
Jung-kang Jin ◽  
Clifford M Hogan ◽  
Christopher C Glembotski
Keyword(s):  
Cell Death ◽  
Heart Disease ◽  
Stress Response ◽  
Ischemic Heart Disease ◽  
Er Stress ◽  
Ischemic Heart ◽  
Neonatal Rat ◽  
Loss Of Function ◽  
Er Stress Response ◽  
Stress Response Genes

Rationale: ATF6α and ATF6β are endoplasmic reticulum (ER) transmembrane proteins that sense the accumulation of toxic misfolded proteins in the ER of cardiomyocytes, which can be brought about by ER stresses as ischemia. Upon ER stress, ATF6α is proteolytically cleaved into a transcription factor that binds to ER stress response elements (ERSEs) and increases expression of cardioprotective genes that restore ER protein folding. If ER proteostasis is not restored, maladaptive signaling is initiated. ATF6β is also proteolytically cleaved during ER stress, binds to the same ERSEs as ATF6α, but does not induce transcription. Hence it is clear from the above studies done in cancer cells that there are some marked similarities and differences between ATF6α and ATF6β. However, the relative roles of ATF6α and ATF6β have not been studied in the heart, where they might work in concert to mediate the dynamic switch from adaptive to maladaptive gene programing during myocardial pathology. Methods: We used neonatal rat ventricular myocytes (NRVMs) to explore the effects of ATF6α or ATF6β loss-of-function in cells treated with the ER stressor, thapsigargin (TG), which mimics ischemic heart disease. Results: In NRVM treated with TG, knockdown of ATF6β resulted in much more pronounced cell death in isolated myocytes than knockdown of ATF6α. Consistent with this finding, transcriptome analyses showed that compared to knocking down ATF6α, knockdown of ATF6β upregulated much more maladaptive, cell death-inducing genes and downregulated more cardioprotective genes. Surprisingly, knockdown of either ATF6α or ATF6β downregulated some common adaptive ER stress response genes, such as GRP78 and Derlin while also upregulating common maladaptive ER stress response genes, such as CHOP, Bcl2, Bax. Conclusion: These data indicate that both ATF6α and ATF6 β are needed for optimal viability of NRVM subjected to ER stress. There is a common, as well as differential gene regulation program controlled by these two isoforms of ATF6. Importantly, this study demonstrates a novel mechanism by which these two isoforms of ATF6 interact to govern the progression from adaptive to maladaptive ER stress signaling during chronic misfolding of ER proteins that occurs in ischemic heart disease.

Tissue Oxygen Transfer During Reperfusion and Post-Conditioning

2011 ◽  
Author(s):  
Anthony J. La Barck ◽  
Jennifer E. Akers ◽  
Thomas L. Merrill
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Reperfusion Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Coronary Intervention ◽  
The United States ◽  
Ischemic Heart ◽  
Area At Risk

Heart disease is the leading cause of death in the United States. Ischemic heart disease occurs when coronary blood flow to the heart is reduced, limiting the amount of oxygen and nutrients the heart receives. When blood flow is restored after a percutaneous transluminal coronary intervention (PCI), rapid reperfusion from sudden balloon deflation can cause further injury to oxygen-starved tissue, leading to increased cell injury and cell death. Studies in animal models with ischemic heart disease have shown that reperfusion injury may account for up to 50% of the final infarct size [1]. Post-conditioning (PC) may reduce the amount of reperfusion injury by applying intermittent periods of ischemia during the early moments of reperfusion. This procedure periodically occludes blood vessels during reperfusion by periodically inflating and deflating an angioplasty balloon according to a specific algorithm. Zhao et al. showed that PC reduced reperfusion injury in a canine model by applying 3 cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia (re-occlusion) at the onset of reperfusion. PC in this study reduced tissue AN/AAR (area of necrosis/area at risk) by 48% [2]. In 2008, Gao et al. demonstrated that the effectiveness of PC in rats was dependent on the number of cycles in the PC algorithm, as well as the durations of the ischemia/reperfusion phases [3].

scholarly journals Medicinal Plants with Cardioprotective Potency and Some Possible Cardiac Biomarkers for Monitoring and Diagnosing Myocardial Infarction: A Review

2021 ◽  
Vol 12 (4) ◽  
pp. 2454-2459
Author(s):  
Ajah O. ◽  
Omodamiro O. D. ◽  
Christian E. Odo
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Heart Disease ◽  
Medicinal Plants ◽  
Ischemic Heart Disease ◽  
Myocardial Cell ◽  
Ischemic Heart ◽  
Cardiac Biomarkers ◽  
Active Components ◽  
Threatening Condition

Following the increasing rate of Cardiovascular diseases, actions have been taken and geared towards the discovery of new leads (drugs) since the existing drugs treat and manage some of these Cardiovascular ailments but with proven adverse effects on the side of the patients. Coronary artery disease which is also called Ischemic heart disease is a crucial problem worldwide, and it's known as a major non-transmissible disease. A good example of ischemic heart disease is acute myocardial infarction (MI), and its manifest due to inequality between coronary blood supply and myocardial demand. Sustained ischemia causes myocardial infarction, which leads to myocardial cell death. Cardiac biomarkers are enzymes/proteins that are used as essential tools in cardiology for primary and secondary prevention, diagnosis and management of acute myocardial infarction and other heart-related issues. The treatment and management of diseases in the African continent are achieved mostly with traditional medicine, and Plants are known to contain active components which possess medical properties that are harnessed for the treatment of different diseases. So many medicinal plants have shown to be potent in the treatment and management of this life-threatening condition known as acute myocardial infarction (heart attack). Some research-proven cardioprotective plants and possible tools for evaluating their potency are reviews in this article.

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