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Mechanosensing and Regulation of Cardiac Function.

Dostal DE, Feng H, Nizamutdinov D, Golden HB, Afroze SH, Dostal JD, Jacob JC, Foster DM, Tong C, Glaser S, Gerilechaogetu F - J Clin Exp Cardiolog (2014)

Bottom Line: The role of mechanical force as an important regulator of structure and function of mammalian cells, tissues, and organs has recently been recognized.Physical stimuli sensed by cells are transmitted through intracellular signal transduction pathways resulting in altered physiological responses or pathological conditions.Integrin link the extracellular matrix and the intracellular cytoskeleton to initiate the mechanical signalling, whereas, the AT1 receptor could be activated by mechanical stress through an angiotensin-II-independent mechanism.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Texas Veterans Health Care System, Temple, Texas, USA ; Division of Molecular Cardiology, Cardiovascular Research Institute, Texas A&M University Health Science Centre, College of Medicine, Temple, Texas, USA.

ABSTRACT
The role of mechanical force as an important regulator of structure and function of mammalian cells, tissues, and organs has recently been recognized. However, mechanical overload is a pathogenesis or comorbidity existing in a variety of heart diseases, such as hypertension, aortic regurgitation and myocardial infarction. Physical stimuli sensed by cells are transmitted through intracellular signal transduction pathways resulting in altered physiological responses or pathological conditions. Emerging evidence from experimental studies indicate that β1-integrin and the angiotensin II type I (AT1) receptor play critical roles as mechanosensors in the regulation of heart contraction, growth and leading to heart failure. Integrin link the extracellular matrix and the intracellular cytoskeleton to initiate the mechanical signalling, whereas, the AT1 receptor could be activated by mechanical stress through an angiotensin-II-independent mechanism. Recent studies show that both Integrin and AT1 receptor and their downstream signalling factors including MAPKs, AKT, FAK, ILK and GTPase regulate heart function in cardiac myocytes. In this review we describe the role of mechanical sensors residing within the plasma membrane, mechanical sensor induced downstream signalling factors and its potential roles in cardiac contraction and growth.

No MeSH data available.


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Schematic of regulation of cardiac myocytes function by mechanical stretch.
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Figure 1: Schematic of regulation of cardiac myocytes function by mechanical stretch.

Mentions: Mechanical stretch can lead to activation angiotensin II type 1 receptor and integrins. Activation of these proteins can initiate several downstream signalling pathways, such as MAPK and AKT, which can alter contractile function by leading to changes in intracellular calcium ion concentration. Abbreviations: AT1R, Angiotensin II Type 1 Receptor; ERK, extracellular signal regulated kinase; JNK, c-jun N-terminal kinase; p38, p38 mitogen activated protein kinase; FAK, focal adhesion kinase; PP2A, protein phosphatase-2 A; RYR, ryanodine receptors; SR, sarcoplasmic reticulum; SERCA, sarcoplasmic reticulum calcium-ATPase (Figure 1).


Mechanosensing and Regulation of Cardiac Function.

Dostal DE, Feng H, Nizamutdinov D, Golden HB, Afroze SH, Dostal JD, Jacob JC, Foster DM, Tong C, Glaser S, Gerilechaogetu F - J Clin Exp Cardiolog (2014)

Schematic of regulation of cardiac myocytes function by mechanical stretch.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255974&req=5

Figure 1: Schematic of regulation of cardiac myocytes function by mechanical stretch.
Mentions: Mechanical stretch can lead to activation angiotensin II type 1 receptor and integrins. Activation of these proteins can initiate several downstream signalling pathways, such as MAPK and AKT, which can alter contractile function by leading to changes in intracellular calcium ion concentration. Abbreviations: AT1R, Angiotensin II Type 1 Receptor; ERK, extracellular signal regulated kinase; JNK, c-jun N-terminal kinase; p38, p38 mitogen activated protein kinase; FAK, focal adhesion kinase; PP2A, protein phosphatase-2 A; RYR, ryanodine receptors; SR, sarcoplasmic reticulum; SERCA, sarcoplasmic reticulum calcium-ATPase (Figure 1).

Bottom Line: The role of mechanical force as an important regulator of structure and function of mammalian cells, tissues, and organs has recently been recognized.Physical stimuli sensed by cells are transmitted through intracellular signal transduction pathways resulting in altered physiological responses or pathological conditions.Integrin link the extracellular matrix and the intracellular cytoskeleton to initiate the mechanical signalling, whereas, the AT1 receptor could be activated by mechanical stress through an angiotensin-II-independent mechanism.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Texas Veterans Health Care System, Temple, Texas, USA ; Division of Molecular Cardiology, Cardiovascular Research Institute, Texas A&M University Health Science Centre, College of Medicine, Temple, Texas, USA.

ABSTRACT
The role of mechanical force as an important regulator of structure and function of mammalian cells, tissues, and organs has recently been recognized. However, mechanical overload is a pathogenesis or comorbidity existing in a variety of heart diseases, such as hypertension, aortic regurgitation and myocardial infarction. Physical stimuli sensed by cells are transmitted through intracellular signal transduction pathways resulting in altered physiological responses or pathological conditions. Emerging evidence from experimental studies indicate that β1-integrin and the angiotensin II type I (AT1) receptor play critical roles as mechanosensors in the regulation of heart contraction, growth and leading to heart failure. Integrin link the extracellular matrix and the intracellular cytoskeleton to initiate the mechanical signalling, whereas, the AT1 receptor could be activated by mechanical stress through an angiotensin-II-independent mechanism. Recent studies show that both Integrin and AT1 receptor and their downstream signalling factors including MAPKs, AKT, FAK, ILK and GTPase regulate heart function in cardiac myocytes. In this review we describe the role of mechanical sensors residing within the plasma membrane, mechanical sensor induced downstream signalling factors and its potential roles in cardiac contraction and growth.

No MeSH data available.


Related in: MedlinePlus