Morphology of the Myoendocrine Cardiac Cell and Extra-Auricular Systems Producing Cardiac Hormones

1989 ◽  
pp. 3-26 ◽  
Author(s):  
W. G. Forssmann ◽  
S. Feller ◽  
M. Meyer ◽  
P. Schulz-Knappe
Keyword(s):  
Cardiac Cell ◽  
Cardiac Hormones

The impact of age on the outcome of cardiac cell therapy

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
B Nasseri ◽  
M Kukucka ◽  
SJ Kim ◽  
YH Choi ◽  
KS Kang ◽  
...  
Keyword(s):  
Cell Therapy ◽  
Cardiac Cell ◽  
Cardiac Cell Therapy ◽  
The Impact

Placenta-derived mesenchymal stem cells for allogenic cardiac cell therapy

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
R Roy ◽  
M Kukucka ◽  
D Messroghli ◽  
A Brodarac ◽  
M Becher ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Therapy ◽  
Cardiac Cell ◽  
Cardiac Cell Therapy

Hox-Dependent Coordination of Cardiac Cell Patterning and Differentiation

2019 ◽  
Author(s):  
Sonia Stefanovic ◽  
Brigitte Laforest ◽  
Jean-Pierre Desvignes ◽  
Fabienne Lescroart ◽  
Laurent Argiro ◽  
...  
Keyword(s):  
Cell Patterning ◽  
Cardiac Cell

Diabetic Cardiomyopathy: From Mechanism to Management in a Nutshell

2020 ◽  
Vol 20 ◽  
Author(s):  
Shahzad Khan ◽  
Syed S. Ahmad ◽  
Mohammad A. Kamal
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Immune Modulation ◽  
Cell Injury ◽  
Interstitial Fibrosis ◽  
Systolic Dysfunction ◽  
Therapeutic Strategies ◽  
Cardiac Cell ◽  
Clinical Heart Failure ◽  
Artery Disease ◽  
Apoptosis And Necrosis

: Diabetic cardiomyopathy (DCM) is a significant complication of diabetes mellitus characterized by gradual failing heart with detrimental cardiac remodellings such as fibrosis and diastolic and systolic dysfunction, which is not directly attributable to coronary artery disease. Insulin resistance and resulting hyperglycemia is the main trigger involved in the initiation of diabetic cardiomyopathy. There is a constellation of many pathophysiological events such as lipotoxicity, oxidative stress, inflammation, inappropriate activation of the renin-angiotensin-aldosterone system, dysfunctional immune modulation promoting increased rate of cardiac cell injury, apoptosis, and necrosis which ultimately culminates into interstitial fibrosis, cardiac stiffness, diastolic dysfunction initially and later systolic dysfunction too. These events finally lead to clinical heart failure of DCM. Herein, we have briefly discussed the pathophysiology of DCM. We have also briefly mentioned potential therapeutic strategies currently used for DCM.

Cardiac Hormones Activate ERK 1/2 Kinases in Human Fibroblasts

2008 ◽  
Vol 41 (03) ◽  
pp. 197-201 ◽  
Author(s):  
Y. Sun ◽  
E. Eichelbaum ◽  
H. Wang ◽  
D. Vesely
Keyword(s):  
Human Fibroblasts ◽  
Cardiac Hormones

scholarly journals The Cardiovascular Phenotype in Fabry Disease: New Findings in the Research Field

2021 ◽  
Vol 22 (3) ◽  
pp. 1331
Author(s):  
Daniela Sorriento ◽  
Guido Iaccarino
Keyword(s):  
Fabry Disease ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Research Field ◽  
Cardiac Cell ◽  
Lysosomal Storage ◽  
Clinical Level ◽  
New Findings ◽  
Alpha Gene ◽  
Alpha Galactosidase

Fabry disease (FD) is a lysosomal storage disorder, depending on defects in alpha-galactosidase A (GAL) activity. At the clinical level, FD shows a high phenotype variability. Among them, cardiovascular dysfunction is often recurrent or, in some cases, is the sole symptom (cardiac variant) representing the leading cause of death in Fabry patients. The existing therapies, besides specific symptomatic treatments, are mainly based on the restoration of GAL activity. Indeed, mutations of the galactosidase alpha gene (GLA) cause a reduction or lack of GAL activity leading to globotriaosylceramide (Gb3) accumulation in several organs. However, several other mechanisms are involved in FD’s development and progression that could become useful targets for therapeutics. This review discusses FD’s cardiovascular phenotype and the last findings on molecular mechanisms that accelerate cardiac cell damage.

Fluorescence and differential light absorption recordings with calcium probes and potential-sensitive dyes in skinned cardiac cells

1982 ◽  
Vol 60 (4) ◽  
pp. 556-567 ◽  
Author(s):  
Alexandre Fabiato
Keyword(s):  
Cardiac Cells ◽  
Arsenazo Iii ◽  
Optical Methods ◽  
Cardiac Cell ◽  
Differential Absorption ◽  
Fluorescence Measurements ◽  
Merocyanine 540 ◽  
Inverted Microscope ◽  
Optimum Wavelength ◽  
Absorption Measurements

This report describes an optical system for microspectrophotometry in a single cardiac cell from which the sarcolemma has been removed by microdissection (skinned cardiac cell). This system is attached to the high power inverted microscope used for the microdissection and includes (a) a single variable wavelength microspectrophotometer used to define the spectrum of a given dye or Ca2+ probe; and (b) a dual wavelength, differential microspectrophotometer used to record differentially between the optimum wavelength and a wavelength separated by 25–30 nm. Results are presented using the following optical methods: (a) fluorescence measurements with chlorotetracycline to monitor the amount of Ca2+ bound to the inner face of the sarcoplasmic reticulum (SR) membrane; (b) differential absorption measurements with arsenazo III to measure changes of myoplasmic [Ca2+]free resulting from Ca2+ release from the SR; (c) fluorescence and (or) differential absorption measurements with the potential-sensitive dyes merocyanine 540, NK 2367, and di-S-C3(5) to monitor changes of charge distribution on the SR membrane during Ca2+ accumulation in the SR, as well as before and during Ca2+-induced release of Ca2+ from the SR. A small and rapid signal is observed which precedes the Ca2+-induced release of Ca2+ from the SR. It is detected as an increase of Ca2+ binding inside the SR with chlorotetracycline and as a "hyperpolarization" with potential-sensitive dyes, while no transient change of myoplasmic [Ca2+]free is detected with arsenazo III. This small and rapid signal preceding the Ca2+ release may be a first hint to an understanding of the mechanism whereby a small increase of [Ca2+]free outside the SR triggers Ca2+ release from the SR.

Sign in / Sign up

Export Citation Format

Share Document