vascular repair
Recently Published Documents


TOTAL DOCUMENTS

356
(FIVE YEARS 67)

H-INDEX

38
(FIVE YEARS 5)

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 183
Author(s):  
Colin E. Evans

Inflammatory lung injury is characterized by lung endothelial cell (LEC) death, alveolar epithelial cell (AEC) death, LEC–LEC junction weakening, and leukocyte infiltration, which together disrupt nutrient and oxygen transport. Subsequently, lung vascular repair is characterized by LEC and AEC regeneration and LEC–LEC junction re-annealing, which restores nutrient and oxygen delivery to the injured tissue. Pulmonary hypoxia is a characteristic feature of several inflammatory lung conditions, including acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and severe coronavirus disease 2019 (COVID-19). The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs) 1 and 2. These transcription factors control the expression of a wide variety of target genes, which in turn mediate key pathophysiological processes including cell survival, differentiation, migration, and proliferation. HIF signaling in pulmonary cell types such as LECs and AECs, as well as infiltrating leukocytes, tightly regulates inflammatory lung injury and repair, in a manner that is dependent upon HIF isoform, cell type, and injury stimulus. The aim of this review is to describe the HIF-dependent regulation of inflammatory lung injury and vascular repair. The review will also discuss potential areas for future study and highlight putative targets for inflammatory lung conditions such as ALI/ARDS and severe COVID-19. In the development of HIF-targeted therapies to reduce inflammatory lung injury and/or enhance pulmonary vascular repair, it will be vital to consider HIF isoform- and cell-specificity, off-target side-effects, and the timing and delivery strategy of the therapeutic intervention.


2022 ◽  
Vol 124 (1) ◽  
pp. 151833
Author(s):  
Fanchen Yan ◽  
Xiaodan Liu ◽  
Huang Ding ◽  
Wei Zhang

2021 ◽  
Vol 12 ◽  
Author(s):  
Mingyan Wang ◽  
Wei Zhang ◽  
Zhi Qi

Platelets deposition at the site of vascular injury is a key event for the arrest of bleeding and for subsequent vascular repair. Therefore, the regulation of platelet deposition onto the injured site during the process of platelet plug formation is an important event. Herein, we showed that electrical signal could regulate the deposition of platelets onto the injured site. On the one hand, the area of platelet deposition was reduced when the cathode of the applied electric field was placed at the injured site beforehand, while it was increased when the anode was at the site. On the other hand, if a cathode was placed at the injured site after the injury, the electrical signal could remove the outer layer of the deposited platelets. Furthermore, an electric field could drive rapid platelet deposition onto the blood vessel wall at the site beneath the anode even in uninjured blood vessels. Platelet deposition could thus be manipulated by externally applied electric field, which might provide a mechanism to drive platelet deposition onto the wall of blood vessels.


2021 ◽  
Author(s):  
Pilar Jimenez-Quevedo ◽  
Esther Bernardo ◽  
Maria del Trigo ◽  
Shuji Otsuki ◽  
Luis Nombela-Franco ◽  
...  

2021 ◽  
Vol 143 ◽  
pp. 112200
Author(s):  
Ruili Guo ◽  
Xue Wang ◽  
Yani Fang ◽  
Xiongjian Chen ◽  
Kun Chen ◽  
...  

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
J Rodriguez-Carrio ◽  
R Bangueses ◽  
I Rodriguez ◽  
M Pevida ◽  
S Llames ◽  
...  

Abstract Background In-stent restenosis (ISR) is a major challenge in patients with coronary artery disease due to its association with poor clinical outcomes, quality of life and costs. ISR etiopathogenesis remains unclear, but traditional risk factors cannot fully explain ISR burden. Inflammation-driven loss of endothelial homeostasis and neoatherosclerosis are thought to hallmark ISR. Recently, a number of immune cell subsets have been related to vascular repair failure and endothelial damage, such as angiogenic T-cells (Tang), endothelial progenitor cells (EPC), senescent T-cells (CD4+CD28null), monocyte subsets and low-density granulocytes (LDG). However, these subsets have not been studied in ISR and an integrative analysis is lacking. Purpose 1) to evaluate potential alterations in vascular repair and endothelial damage cellular mediators in ISR and 2) to identify profiles associated with clinical features. Methods Case-control study including 30 patients with ≥1 previous stent implantation (15 bare metal stents (BMS) and 15 drug-eluting stents (DE)) which suffered restenosis and 30 patients with ≥1 BMS without restenosis, both confirmed in a second angiogram performed by clinical symptoms >8 months after index procedure. Cellular mediators of vascular homeostasis were quantified by flow cytometry based on their surface markers in peripheral blood (EPC: CD34+VEGFR2+CD133+; EC: CD34-VEGFR+CD133-; Tang: CD3+CD31+CXCR4+; senescent T-cells: CD4+CD28null) or in peripheral blood mononuclear cells (monocyte subsets, ACE expression; total LDG: CD15+; and LDG subsets: CD15+CD14-CD16- and CD15+CD14lowCD16+). Results Patients with ISR exhibited decreased circulating Tang (p=0.005) and EPC (p<0.001), whereas CD4+CD28null and EC counts were higher (p<0.0001 and p=0.006) compared to ISR-free patients. No differences were observed in the frequency of monocyte subsets (all p>0.050), although ACE expression was found to be increased (non-classical p<0.001; and intermediate p<0.0001) in ISR. Moreover, no differences were noted in the total LDG population (p=0.092), but an increase in the CD14- compartment was observed in ISR (p=0.004). An unsupervised cluster analysis built with these subsets informed the presence of three profiles (Figure 1): group I (hallmarked by a profound impairment in vascular repair and augmented damage, suggestive of central haematopoiesis traits) exhibited an enhanced clinical risk profile compared to group II (hallmarked by a mid-altered vascular repair) and group III (hallmarked by CD16+ shifted LDG and ACE expression) (Figure 2). No differences were observed in stent types or traditional risk factors but hypertension. Conclusions Profound alterations in immune populations related to vascular repair and endothelial damage are found in ISR. Distinct cellular profiles can be distinguished within ISR, suggesting that different alterations may uncover different ISR clinical phenotypes, in terms of severity and extension. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): ISCIIIPrograma Intramural ISPA Figure 1 Figure 2


Author(s):  
Panagiotis Mastorakos ◽  
Matthew V. Russo ◽  
Tianzan Zhou ◽  
Kory Johnson ◽  
Dorian B. McGavern

Sign in / Sign up

Export Citation Format

Share Document