Cardiac Physiology Review

2008 ◽  
pp. 1-16
Author(s):  
Brian Feingold ◽  
Ricardo Munoz
Keyword(s):  
Cardiac Physiology

scholarly journals Impact of Aldosterone on the Failing Myocardium: Insights from Mitochondria and Adrenergic Receptors Signaling and Function

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1552
Author(s):  
Mariona Guitart-Mampel ◽  
Pedro Urquiza ◽  
Jordana I. Borges ◽  
Anastasios Lymperopoulos ◽  
Maria E. Solesio
Keyword(s):  
Mitochondrial Dysfunction ◽  
G Protein ◽  
Adrenergic Receptor ◽  
Cellular Level ◽  
Cardiac Physiology ◽  
Failing Heart ◽  
Receptor Kinases ◽  
And Function ◽  
The Impact ◽  
G Protein Coupled

The mineralocorticoid aldosterone regulates electrolyte and blood volume homeostasis, but it also adversely modulates the structure and function of the chronically failing heart, through its elevated production in chronic human post-myocardial infarction (MI) heart failure (HF). By activating the mineralocorticoid receptor (MR), a ligand-regulated transcription factor, aldosterone promotes inflammation and fibrosis of the heart, while increasing oxidative stress, ultimately induding mitochondrial dysfunction in the failing myocardium. To reduce morbidity and mortality in advanced stage HF, MR antagonist drugs, such as spironolactone and eplerenone, are used. In addition to the MR, aldosterone can bind and stimulate other receptors, such as the plasma membrane-residing G protein-coupled estrogen receptor (GPER), further complicating it signaling properties in the myocardium. Given the salient role that adrenergic receptor (ARs)—particularly βARs—play in cardiac physiology and pathology, unsurprisingly, that part of the impact of aldosterone on the failing heart is mediated by its effects on the signaling and function of these receptors. Aldosterone can significantly precipitate the well-documented derangement of cardiac AR signaling and impairment of AR function, critically underlying chronic human HF. One of the main consequences of HF in mammalian models at the cellular level is the presence of mitochondrial dysfunction. As such, preventing mitochondrial dysfunction could be a valid pharmacological target in this condition. This review summarizes the current experimental evidence for this aldosterone/AR crosstalk in both the healthy and failing heart, and the impact of mitochondrial dysfunction in HF. Recent findings from signaling studies focusing on MR and AR crosstalk via non-conventional signaling of molecules that normally terminate the signaling of ARs in the heart, i.e., the G protein-coupled receptor-kinases (GRKs), are also highlighted.

Sub-lethal Camphor Exposure Triggers Oxidative Stress, Cardiotoxicity, and Cardiac Physiology Alterations in Zebrafish Embryos

2021 ◽  
Author(s):  
Zheng-Cai Du ◽  
Zhong-Shang Xia ◽  
Ming-Zhe Zhang ◽  
Yan-Ting Wei ◽  
Nemi Malhotra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zebrafish Embryos ◽  
Cardiac Physiology

scholarly journals S100A9 is a functional effector of infarct wall thinning after myocardial infarction

2021 ◽  
Author(s):  
Upendra Chalise ◽  
Mediha Becirovic-Agic ◽  
Michael J Daseke II ◽  
Shelby R. Konfrst ◽  
Jocelyn R. Rodriguez-Paar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Neutrophil Infiltration ◽  
Vehicle Control ◽  
Macrophage Infiltration ◽  
Secreted Protein ◽  
Cardiac Physiology ◽  
Wall Thinning ◽  
Saline Vehicle ◽  
Lower Ejection Fraction

Neutrophils infiltrate into the left ventricle (LV) early after myocardial infarction (MI) and launch a pro-inflammatory response. Along with neutrophil infiltration, LV wall thinning due to cardiomyocyte necrosis also peaks at day 1 in the mouse model of MI. To understand the correlation, we examined a previously published dataset that included day 0 (n=10) and MI day 1 (n=10) neutrophil proteome and echocardiography assessments. Out of 123 proteins, 4 proteins positively correlated with the infarct wall thinning index (1/wall thickness): histone 1.2 (r=0.62, p=0.004), S100A9 (r=0.60, p=0.005), histone 3.1 (r=0.55, p=0.01), and fibrinogen (r=0.47, p=0.04). As S100A9 was the highest ranked secreted protein, we hypothesized that S100A9 is a functional effector of infarct wall thinning. We exogenously administered S100A8/A9 at the time of MI to mice (C57BL/6J, male, 3-6 months of age, n=7M (D1), and n=5M (D3)) and compared to saline vehicle control treated mice (n=6M (D1) and n=6M (D3)) at MI days 1 and 3. At MI day 3, the S100A8/A9 group showed a 22% increase in the wall thinning index compared to saline (p=0.02), along with higher dilation and lower ejection fraction. The decline in cardiac physiology occurred subsequent to increased neutrophil and macrophage infiltration at MI day 1 and increased macrophage infiltration at D3. Our results reveal that S100A9 is a functional effector of infarct wall thinning.

Extracellular Matrix Communication and Turnover in Cardiac Physiology and Pathology

2015 ◽  
pp. 687-719 ◽  
Author(s):  
Abhijit Takawale ◽  
Siva S.V.P. Sakamuri ◽  
Zamaneh Kassiri
Keyword(s):  
Extracellular Matrix ◽  
Cardiac Physiology

scholarly journals Hyperthyroidism Evokes Myocardial Ceramide Accumulation

2015 ◽  
Vol 35 (2) ◽  
pp. 755-766 ◽  
Author(s):  
Agnieszka Mikłosz ◽  
Bartłomiej Łukaszuk ◽  
Adrian Chabowski ◽  
Filip Rogowski ◽  
Krzysztof Kurek ◽  
...  
Keyword(s):  
Peroxisome Proliferator ◽  
Cardiac Physiology ◽  
Peroxisome Proliferator Activated Receptor ◽  
Sphingosine 1 Phosphate ◽  
Male Wistar Rats ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Cpt I ◽  
Amp Activated Protein Kinase ◽  
Ceramide Accumulation

Background: Thyroid hormones (THs) are key regulators of cardiac physiology as well as modulators of different cellular signals including the sphingomyelin/ceramide pathway. The objective of this study was to examine the effect of hyperthyroidism on the metabolism of sphingolipids in the muscle heart. Methods: Male Wistar rats were treated for 10 days with triiodothyronine (T3) at a dose of 50µg/100g of body weight. Animals were then anaesthetized and samples of the left ventricle were excised. Results: We have demonstrated that prolonged, in vivo, T3 treatment increased the content of sphinganine (SFA), sphingosine (SFO), ceramide (CER) and sphingomyelin (SM), but decreased the level of sphingosine-1-phosphate (S1P) in cardiac muscle. Accordingly, the changes in sphingolipids content were accompanied by a lesser activity of neutral sphingomyelinase and without significant changes in ceramidases activity. Hyperthyroidism also induced activation of AMP-activated protein kinase (AMPK) with subsequently increased expression of mitochondrial proteins: cytochrome c oxidase IV (COX IV), β-hydroxyacyl-CoA dehydrogenase (β-HAD), carnityne palmitoyltransferase I (CPT I) and nuclear peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α). Conclusions: We conclude that prolonged T3 treatment increases sphingolipids metabolism which is reflected by higher concentration of SFA and CER in heart muscle. Furthermore, hyperthyroidism-induced increase in heart sphingomyelin (SM) concentration might be one of the mechanisms underlying maintenance of CER at relatively low level by its conversion to SM together with decreased S1P content.

HUMAN iPSC ENGINEERED CARDIAC TISSUE PLATFORM FAITHFULLY MODELS IMPORTANT CARDIAC PHYSIOLOGY

2021 ◽  
Author(s):  
Willem J. de Lange ◽  
Emily T. Farrell ◽  
Caroline R. Kreitzer ◽  
Derek R. Jacobs ◽  
Di Lang ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
Human Myocardium ◽  
Protein Isoforms ◽  
Calcium Handling ◽  
Unintended Effects ◽  
Cardiac Physiology ◽  
Adrenergic Stimulation ◽  
Cardiac Model ◽  
Short Period ◽  
Tubular System

Cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CM) may provide an important bridge between animal models and intact human myocardium. Fulfilling this potential is hampered by their relative immaturity. hiPSC-CMs grown in monolayer culture lack a t-tubular system, have rudimentary intracellular calcium-handling systems, express predominantly embryonic sarcomeric protein isoforms, and preferentially use glucose as energy substrate. Culturing hiPSC-CM in a 3D environment and the addition of nutritional, pharmacologic and electromechanical stimuli have proven to be beneficial for maturation. We present an assessment of a model in which hiPSC-CMs and hiPSC-derived cardiac fibroblasts are co-cultured in a 3D fibrin matrix to form human engineered cardiac tissue constructs (hECT).The hECT respond to physiological stimuli, including stretch, frequency and β-adrenergic stimulation, develop a t-tubular system, and demonstrate calcium-handling and contractile kinetics that compare favorably with ventricular human myocardium. Transcript levels of genes involved in calcium-handling and contraction are increased. These markers of maturation become more robust over a short period of time in culture (6 weeks vs. 2 weeks in hECT). A comparison of the hECT molecular and performance variables with those of human cardiac tissue and other available engineered tissue platforms is provided to highlight strengths and weaknesses of these preparations. Important and noteworthy aspects of this human cardiac model system are its reliance on 'off-the-shelf' equipment, ability to provide detailed physiological performance data, and the ability to achieve a relatively mature cardiac physiology without additional nutritional, pharmacological and electromechanical stimuli that may elicit unintended effects on function.

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