Progenitor Cells and Clinical Outcomes in Patients With Acute Coronary Syndromes

Tahhan, Ayman Samman; Hammadah, Muhammad; Raad, Mohamad; Almuwaqqat, Zakaria; Alkhoder, Ayman; Sandesara, Pratik B.; Mohamed-Kelli, Heval; Hayek, Salim S.; Kim, Jeong Hwan; O’Neal, Wesley T.; Topel, Matthew; Grant, Aubrey J.; Sabbak, Nabil; Heinl, Robert E.; Gafeer, Mohamad Mazen; Obideen, Malik; Kaseer, Belal; Abdelhadi, Nasser; Ko, Yi‐An; Liu, Chang; Hesaroieh, Iraj; Mahar, Ernestine; Vaccarino, Viola; Waller, Edmund K.; Quyyumi, Arshed A.

doi:10.1161/circresaha.118.312821

Cited by 34 publications

(32 citation statements)

References 51 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of the present study may have implications in the pathogenesis of thrombotic manifestations in BS. Indeed, CPC have not only been associated with coronary artery disease (54) and atherosclerosis (55). Different from other inflammatory immune-mediated conditions, BS is not associated with accelerated atherosclerosis, despite without having a clear pathogenetic explanation (56).…”

Section: Discussionmentioning

confidence: 99%

Stem-Cell-Derived Circulating Progenitors Dysfunction in Behçet's Syndrome Patients Correlates With Oxidative Stress

et al. 2019

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Stem-Cell-Derived Circulating Progenitors Dysfunction in Behçet's Syndrome Patients Correlates With Oxidative Stress

et al. 2019

View full text Add to dashboard Cite

“…It has been hypothesized that mobilization of MPCs/EPCs and increase in growth and differentiation into mature cells in vasculature accompany acute events, including AMI and acute HF, and are associated with vascular reparation [219,220]. However, previous acute CV events and chronic metabolic and CV diseases, such as diabetes mellitus, abdominal obesity, and hypertension, were reported to be causes of an exhausting pool of circulating angiopoetic MPCs/EPCs with immune phenotypes CD45+CD34+, CD45+CD34+CD133+, and CD45+CD34+CD133+CD184+ [221].…”

Section: Circulating Mononuclear and Endothelial Progenitormentioning

confidence: 99%

Adverse Cardiac Remodelling after Acute Myocardial Infarction: Old and New Biomarkers

Berezin

2020

Disease Markers

View full text Add to dashboard Cite

The prevalence of heart failure (HF) due to cardiac remodelling after acute myocardial infarction (AMI) does not decrease regardless of implementation of new technologies supporting opening culprit coronary artery and solving of ischemia-relating stenosis with primary percutaneous coronary intervention (PCI). Numerous studies have examined the diagnostic and prognostic potencies of circulating cardiac biomarkers in acute coronary syndrome/AMI and heart failure after AMI, and even fewer have depicted the utility of biomarkers in AMI patients undergoing primary PCI. Although complete revascularization at early period of acute coronary syndrome/AMI is an established factor for improved short-term and long-term prognosis and lowered risk of cardiovascular (CV) complications, late adverse cardiac remodelling may be a major risk factor for one-year mortality and postponded heart failure manifestation after PCI with subsequent blood flow resolving in culprit coronary artery. The aim of the review was to focus an attention on circulating biomarker as a promising tool to stratify AMI patients at high risk of poor cardiac recovery and developing HF after successful PCI. The main consideration affects biomarkers of inflammation, biomechanical myocardial stress, cardiac injury and necrosis, fibrosis, endothelial dysfunction, and vascular reparation. Clinical utilities and predictive modalities of natriuretic peptides, cardiac troponins, galectin 3, soluble suppressor tumorogenicity-2, high-sensitive C-reactive protein, growth differential factor-15, midregional proadrenomedullin, noncoding RNAs, and other biomarkers for adverse cardiac remodelling are discussed in the review.

show abstract

“…The results of clinical trials of stem cell and progenitor cell treatments for ischemic diseases in elderly subjects have been disappointing [22]. Samman Tahhan and colleagues recently reported a close relationship between circulating progenitor cells and clinical outcomes in elderly patients with acute coronary syndrome [23]. It is thus necessary to determine what improves the mobilization and function of EPCs in aging.…”

Section: Introductionmentioning

confidence: 99%

Cathepsin K Deficiency Impaired Ischemia-Induced Neovascularization in Aged Mice

Yue

Jiang

et al. 2020

Stem Cells International

View full text Add to dashboard Cite

Background. Aging is a major risk factor for cardiovascular disease. Cysteine protease cathepsin K (CatK) has been implicated in the process of angiogenesis, but the exact roles of individual CatK in vessel formation during aging are poorly understood. Methods and Results. To study the putative role of CatK in ischemia-induced angiogenesis, we applied a hindlimb ischemia model to aged wild-type (CatK+/+) and CatK-deficient (CatK−/−) mice. A serial laser Doppler blood-flow analysis revealed that the recovery of the ischemic/normal blood-flow ratio in the aged CatK−/−mice was impaired throughout the follow-up period. On postoperative day 14, CatK deficiency had also impaired capillary formation. CatK deficiency reduced the levels of cleaved Notch1, phospho-Akt, and/or vascular endothelial growth factor (VEGF) proteins in the ischemic muscles and bone marrow-derived c-Kit+ cells. A flow cytometry analysis revealed that CatK deficiency reduced the numbers of endothelial progenitor cell (EPC)-like CD31+/c-Kit+ cells in the peripheral blood as well as the ischemic vasculature. In vitro experiments, CatK−/− impaired bone-derived c-Kit+ cellular functions (migration, invasion, proliferation, and tubulogenesis) in aged mice. Our findings demonstrated that aging impaired the ischemia-induced angiogenesis associated with the reductions of the production and mobilization of CD31+/c-Kit+ cells in mice. Conclusions. These findings established that the impairment of ischemia-induced neovascularization in aged CatK−/− mice is due, at least in part, to the reduction of EPC mobilization and the homing of the cells into vasculature that is associated with the impairment of Notch1 signaling activation at advanced ages.

show abstract

Progenitor Cells and Clinical Outcomes in Patients With Acute Coronary Syndromes

Abstract: CPC levels are significantly higher in patients after an AMI compared with those with stable CAD and reflect bone marrow PC content. Among patients with ACS, a lower number of hematopoietic-enriched CPCs are associated with a higher mortality.

Cited by 34 publications

References 51 publications

Stem-Cell-Derived Circulating Progenitors Dysfunction in Behçet's Syndrome Patients Correlates With Oxidative Stress

Stem-Cell-Derived Circulating Progenitors Dysfunction in Behçet's Syndrome Patients Correlates With Oxidative Stress

Adverse Cardiac Remodelling after Acute Myocardial Infarction: Old and New Biomarkers

Cathepsin K Deficiency Impaired Ischemia-Induced Neovascularization in Aged Mice

Contact Info

Product

Resources

About