G Proteins and Heart Failure

Feuerstein, Giora; Rozanski, Dennis J.

doi:10.1161/01.res.87.12.1085

Cited by 10 publications

(1 citation statement)

References 14 publications

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“…G Protein Coupled Receptors (GPCRs) are involved in the signaling pathways controlling cardiovascular remodeling and alterations in Gα protein function is related to heart failure. This also explains the benefits of using antagonists of GPCRs such as β-adrenergic receptor blockers to treat heart failure [ 103 ]. Nix localizes to the mitochondria and sarcoplasmic reticulum, where it influences calcium release and regulates cell death.…”

Section: Alternative Splicing and Apoptotic Genesmentioning

confidence: 99%

Abnormalities in Alternative Splicing of Apoptotic Genes and Cardiovascular Diseases

Dlamini

Tshidino

Hull

2015

IJMS

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Apoptosis is required for normal heart development in the embryo, but has also been shown to be an important factor in the occurrence of heart disease. Alternative splicing of apoptotic genes is currently emerging as a diagnostic and therapeutic target for heart disease. This review addresses the involvement of abnormalities in alternative splicing of apoptotic genes in cardiac disorders including cardiomyopathy, myocardial ischemia and heart failure. Many pro-apoptotic members of the Bcl-2 family have alternatively spliced isoforms that lack important active domains. These isoforms can play a negative regulatory role by binding to and inhibiting the pro-apoptotic forms. Alternative splicing is observed to be increased in various cardiovascular diseases with the level of alternate transcripts increasing elevated in diseased hearts compared to healthy subjects. In many cases these isoforms appear to be the underlying cause of the disease, while in others they may be induced in response to cardiovascular pathologies. Regardless of this, the detection of alternate splicing events in the heart can serve as useful diagnostic or prognostic tools, while those splicing events that seem to play a causative role in cardiovascular disease make attractive future drug targets.

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Section: Alternative Splicing and Apoptotic Genesmentioning

confidence: 99%

Abnormalities in Alternative Splicing of Apoptotic Genes and Cardiovascular Diseases

Dlamini

Tshidino

Hull

2015

IJMS

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Pathways to Myocardial Hypertrophy

Kontaridis

Geladari

2014

Introduction to Translational Cardiovascular Research

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Pathological cardiac hypertrophy occurs as a consequence of adaptive responses to pressure or volume overload, mutations in sarcomeric (or other) proteins, or loss of contractile mass from prior infarction. While initially compensatory, over time when the heart can no longer meet with the increased metabolic demands of the mechanical work load imposed on the heart, dilation and heart failure ensue. Several signaling pathways are critically important in mediating myocardial hypertrophy, including the G-protein coupled receptor, the calcineurin/NFAT, MAPK, and the PI3K/ AKT/mTOR signaling pathways. Importantly, these signaling pathways also control molecular processes, such as cell proliferation, differentiation, survival, migration and other functions of the cell. In addition, the heart is comprised of several cell lineages make up the heart, including cardiomyocytes, fi broblasts, endothelial cells, and vascular smooth muscle cells, each integrally involved in modulating the signaling events that promote the

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Cardiac Hypertrophy

Cokkinos¹

2019

Myocardial Preservation

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G Proteins and Heart Failure

Cited by 10 publications

References 14 publications

Abnormalities in Alternative Splicing of Apoptotic Genes and Cardiovascular Diseases

Abnormalities in Alternative Splicing of Apoptotic Genes and Cardiovascular Diseases

Pathways to Myocardial Hypertrophy

Cardiac Hypertrophy

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