Endothelial Microparticles From Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cell Aging and Thrombogenicity

Abbas, Malak; Jesel, Laurence; Auger, Cyril; Amoura, Lamia; Messas, Nathan; Manin, Guillaume; Rumig, Cordula; León‐González, Antonio J.; Ribeiro, Thais Porto; Silva, Grazielle C.; Abou-Merhi, Raghida; Hamade, Eva; Hecker, Markus; Georg, Yannick; Chakfé, Nabil; Ohlmann, Patrick; Schini‐Kerth, Valérie B.; Toti, Florence; Morel, Olivier

doi:10.1161/circulationaha.116.017513

Cited by 110 publications

(92 citation statements)

References 38 publications

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“…The family of RAS has expanded to include peptides consisting of angiotensin-1-7 [ANG (1-7)], angiotensin-2-8 (ANG III), angiotensin-3-8 (ANG IV), and angiotensin-1-12 [ANG (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)]. ANG (1)(2)(3)(4)(5)(6)(7) is formed by the catalytic action of ACE2 on ANG II and is thought to balance the RAS system by promoting an antagonistic effect on the responses elicited by ANG II-AT 1 R such as vasodilation (278,280). ANG III is produced from ANG II by enzymatic cleavage by an aminopeptidase which fuels similar physiological responses as ANG II (1228).…”

Section: A New and Old Angiotensin Family Ligandsmentioning

confidence: 99%

“…ANG IV is cleaved from ANG III by another aminopeptidase and contributes to blood flow regulation, learning and memory, and neuronal development (363). ANG (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) has been reported to serve as an upstream renin-independent precursor peptide for ANG I and ANG II (15,734). ANG (1-9) is generated from ANG I by several carboxypeptidase-type enzymes, including carboxypeptidase A, cathepsin A, and ACE2 (767).…”

Section: A New and Old Angiotensin Family Ligandsmentioning

confidence: 99%

“…ANG (1-7) has been reported to elicit its effects through the GPCR Mas receptor whereby it mediates antagonistic effects of ANG II, including vasodilation and antihypertensive and antifibrosis effects (800). Similar to Mas activation by ANG (1)(2)(3)(4)(5)(6)(7), alamandine also promotes antihypertensive effects through the Mas-related GPCR member D, MrgD, to produce nitric oxide (NO) (542). Interestingly, MrgD appears to be a second receptor for ANG (1)(2)(3)(4)(5)(6)(7).…”

Section: B Receptors For the Angiotensin Peptidesmentioning

confidence: 99%

“…Alternatively, to maintain chronic ANG II stimulation, one can repeatedly add ANG II to the cell culture. However, rapid conversion of ANG II to ANG III and ANG (1)(2)(3)(4)(5)(6)(7) in culture medium (61) will further complicate the interpretation.…”

Section: Limitations and Pitfalls In Ang II Signaling Researchmentioning

confidence: 99%

“…Production of angiotensin peptides is first initiated by the synthesis and processing of preprorenin in juxtaglomerular cells neighboring the renal glomerulus with subsequent proteolytic cleavage of the signal peptide, intracellular sorting of prorenin to dense-core secretory vesicles, and cleavage of the prosegment, producing catalytically active renin that is secreted in the systemic circulation. Classically, renin cleaves liver-derived angiotensinogen (AGT) into angiotensin I (ANG I), a decapeptide [ANG (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)] which is then further processed by angiotensin-converting enzyme (ACE) into the octapeptide ANG II [Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, ANG (1-8)] (462).…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Forrester

Booz

Sigmund

et al. 2018

Physiological Reviews

816

780

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The renin-angiotensin-aldosterone system plays crucial roles in cardiovascular physiology and pathophysiology. However, many of the signaling mechanisms have been unclear. The angiotensin II (ANG II) type 1 receptor (ATR) is believed to mediate most functions of ANG II in the system. ATR utilizes various signal transduction cascades causing hypertension, cardiovascular remodeling, and end organ damage. Moreover, functional cross-talk between ATR signaling pathways and other signaling pathways have been recognized. Accumulating evidence reveals the complexity of ANG II signal transduction in pathophysiology of the vasculature, heart, kidney, and brain, as well as several pathophysiological features, including inflammation, metabolic dysfunction, and aging. In this review, we provide a comprehensive update of the ANG II receptor signaling events and their functional significances for potential translation into therapeutic strategies. ATR remains central to the system in mediating physiological and pathophysiological functions of ANG II, and participation of specific signaling pathways becomes much clearer. There are still certain limitations and many controversies, and several noteworthy new concepts require further support. However, it is expected that rigorous translational research of the ANG II signaling pathways including those in large animals and humans will contribute to establishing effective new therapies against various diseases.

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Section: A New and Old Angiotensin Family Ligandsmentioning

confidence: 99%

Section: A New and Old Angiotensin Family Ligandsmentioning

confidence: 99%

Section: B Receptors For the Angiotensin Peptidesmentioning

confidence: 99%

Section: Limitations and Pitfalls In Ang II Signaling Researchmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Forrester

Booz

Sigmund

et al. 2018

Physiological Reviews

816

780

View full text Add to dashboard Cite

show abstract

Determinants and treatments of heart failure after transcatheter aortic valve implantation: moving up a notch

et al. 2023

Self Cite

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Transcatheter aortic valve implantation (TAVI) has become an alternative to surgical aortic valve replacement for patients with symptomatic severe aortic stenosis in elderly and comorbid population. Significant improvement in heart function has been observed in patients undergoing TAVI, but numerous patients are readmitted to hospital for heart failure (HF). Moreover, repeat HF hospitalization is strongly associated with an adverse prognosis and increases the financial burden of health care. Although studies have identified pre-existing and post-procedural factors that contribute to HF hospitalization after TAVI, there is a paucity of data regarding optimal post-procedural pharmacological treatments. This review aims to provide an overview of the current understanding of mechanisms, determinants, and potential treatments of HF following TAVI. We first review the pathophysiology of left ventricular (LV) remodelling, coronary microcirculation disorder, and endothelial dysfunction in patients with aortic stenosis and then examine the impact of TAVI on these conditions. We then present evidence of various factors and complications that may interplay with LV remodelling and contribute to HF events after TAVI. Next, we describe the triggers and predictors of early and late HF rehospitalizations following TAVI. Lastly, we discuss the potential of conventional pharmacological treatments, including renin-angiotensin blockers, beta-blockers, and diuretics in TAVI patients. The paper explores the potential of newer drugs, including sodium-glucose co-transporter 2 inhibitors, anti-inflammatory drugs, and ion supplementation. Comprehensive knowledge in this field may aid in recognizing successful existing therapies, developing effective new treatments, and establishing dedicated patient care strategies during follow-up after TAVI.

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Vascular response and intrastent thrombus in the early phase after drug‐eluting versus bare‐metal stent implantation in patients with ST‐segment elevation myocardial infarction: An observational, single‐center study

Sato

Minami

Shimohama

et al. 2018

Health Science Reports

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Background and ObjectivesSecond‐generation drug‐eluting stents (G2‐DES) are associated with a lower rate of acute and subacute stent thrombosis compared with bare‐metal stent (BMS) in the setting of ST‐segment elevation myocardial infarction (STEMI). In this study, our aim was to compare the vascular response and thrombus burden between G2‐DES and BMS in early‐phase STEMI.MethodsBetween May 2010 and August 2014, a total of 41 STEMI patients treated by either G2‐DES (n = 26; everolimus‐eluting stent [EES]: n = 15, zotarolimus‐eluting stent [ZES]: n = 11) or BMS (n = 15) and, with multivessel disease requiring additional percutaneous coronary intervention (PCI), were prospectively enrolled. Optical coherence tomography (OCT) imaging was performed at 1 month after stent implantation.ResultsBaseline clinical characteristics, except for age (61.5 ± 9.3 vs 69.3 ± 9.8, P = 0.01, t test), were comparable between patients with drug‐eluting stent (DES) and BMS. The incidence of residual thrombus after the stent implantation for STEMI was comparable between DES and BMS (7.7% vs 6.7%, P = 0.88, χ 2 test). At 1 month, thrombus burden, defined as the mean thrombus area divided by the mean lumen area, was significantly smaller with DES than with BMS (median interquartile range (IQR), 1.2 (0.0, 1.0) vs 1.2 (0.0, 2.2), P = 0.04, Mann‐Whitney U test), despite a similar percentage of malapposed (median (IQR), 6.2 (2.4, 9.0) vs 2.6 (0.0, 5.8)%, P = 0.07, Mann‐Whitney U test) or uncovered struts (median (IQR), 6.8 (1.8, 13.1) vs 6.14 (2.8, 18.5)%, P = 0.45, Mann‐Whitney U test). No significant difference in thrombus burden was observed between EES and ZES.ConclusionsThrombus burden was significantly smaller with DES than with BMS at 1‐month follow‐up in STEMI cases, although the percentage of malapposed or uncovered struts was similar between the groups. This may partly explain the lower rate of acute and subacute stent thrombosis in G2‐DES that has previously been reported in the literature.

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Endothelial Microparticles From Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cell Aging and Thrombogenicity

Cited by 110 publications

References 38 publications

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Determinants and treatments of heart failure after transcatheter aortic valve implantation: moving up a notch

Vascular response and intrastent thrombus in the early phase after drug‐eluting versus bare‐metal stent implantation in patients with ST‐segment elevation myocardial infarction: An observational, single‐center study

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