β-Adrenergic receptor, an essential target in cardiovascular diseases

Ali, Daniel; Naveed, Muhammad; Gordon, Andrew S.; Majeed, Fatima; Saeed, Muhammad; Ogbuke, Michael I.; Atif, Muhammad; Zubair, Hafiz Muhammad; Li, Changxing

doi:10.1007/s10741-019-09825-x

Cited by 49 publications

(27 citation statements)

References 96 publications

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“…In search of molecular mechanisms through which C3a causes mitochondrial dysfunction, we focused our attention on the cAMP signaling known to be regulated by the activation of G protein-coupled receptors, including C3aR (41,57). A number of studies have described that cAMP had a role in the maintenance of podocyte functional integrity (58,59) and that activating the cAMP signaling limited podocyte mitochondrial fission and apoptosis in response to adriamycin (42).…”

Section: Discussionmentioning

confidence: 99%

C3a receptor blockade protects podocytes from injury in diabetic nephropathy

et al. 2020

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Section: Discussionmentioning

confidence: 99%

C3a receptor blockade protects podocytes from injury in diabetic nephropathy

et al. 2020

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“…The response to EPI and NE is mediated by a set of G protein-coupled adrenergic receptors (ARs), α and/or β-adrenergic receptors, that are targets for several cardiovascular drugs [ 37 , 40 ]. DA receptors are all members of the G protein-coupled receptor family and they are divided into two subtypes: D1-like receptors coupled with Gs alpha subunit (Gs) (D1 and D5) and D2-like receptors coupled with Gi alpha subunit (Gi) (D2, D3, D4).…”

Section: Catecholaminesmentioning

confidence: 99%

Depression and Cardiovascular Disease: The Viewpoint of Platelets

Amadio

Zara

Sandrini

et al. 2020

IJMS

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Depression is a major cause of morbidity and low quality of life among patients with cardiovascular disease (CVD), and it is now considered as an independent risk factor for major adverse cardiovascular events. Increasing evidence indicates not only that depression worsens the prognosis of cardiac events, but also that a cross-vulnerability between the two conditions occurs. Among the several mechanisms proposed to explain this interplay, platelet activation is the more attractive, seeing platelets as potential mirror of the brain function. In this review, we dissected the mechanisms linking depression and CVD highlighting the critical role of platelet behavior during depression as trigger of cardiovascular complication. In particular, we will discuss the relationship between depression and molecules involved in the CVD (e.g., catecholamines, adipokines, lipids, reactive oxygen species, and chemokines), emphasizing their impact on platelet activation and related mechanisms.

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“…In the heart, β-adrenergic (β-AR) receptors are among the most important GPCRs that enhance myocardial performance in response to stress or exercise. β-ARs are activated by catecholamines (adrenaline, noradrenaline) and exist as three subtypes in the heart, from which subtypes β1- and β2- ARs activate Gs proteins (stimulatory G proteins), leading to cAMP formation while β2 also signals through G i/o (inhibitory G proteins) [ 50 , 51 ]. Although cardiac β3-AR has not been described in detail yet, it is coupled to G i/o proteins and NOS-dependent production of cGMP [ 52 ].…”

Section: Epac Compartmentationmentioning

confidence: 99%

Role of EPAC1 Signalosomes in Cell Fate: Friends or Foes?

Formoso

Lezoualc’h

Mialet‐Perez

2020

Cells

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The compartmentation of signaling processes is accomplished by the assembly of protein complexes called signalosomes. These signaling platforms colocalize enzymes, substrates, and anchoring proteins into specific subcellular compartments. Exchange protein directly activated by cAMP 1 (EPAC1) is an effector of the second messenger, 3′,5′-cyclic adenosine monophosphate (cAMP) that is associated with multiple roles in several pathologies including cardiac diseases. Both EPAC1 intracellular localization and molecular partners are key players in the regulation of cell fate, which may have important therapeutic potential. In this review, we summarize the recent findings on EPAC1 structure, regulation, and pharmacology. We describe the importance of EPAC1 subcellular distribution in its biological action, paying special attention to its nuclear localization and mechanism of action leading to cardiomyocyte hypertrophy. In addition, we discuss the role of mitochondrial EPAC1 in the regulation of cell death. Depending on the cell type and stress condition, we present evidence that supports either a protective or detrimental role of EPAC1 activation.

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β-Adrenergic receptor, an essential target in cardiovascular diseases

Cited by 49 publications

References 96 publications

C3a receptor blockade protects podocytes from injury in diabetic nephropathy

C3a receptor blockade protects podocytes from injury in diabetic nephropathy

Depression and Cardiovascular Disease: The Viewpoint of Platelets

Role of EPAC1 Signalosomes in Cell Fate: Friends or Foes?

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