Role of microRNAs in endothelial inflammation and senescence

Qin, Bing; Yang, Huan; Xiao, Bo

doi:10.1007/s11033-011-1241-0

Cited by 86 publications

(91 citation statements)

References 82 publications

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“…Decreased level of miR‐221s in healthy old individuals, is sufficient to increase the expression of their predicted targets; PI3K and c‐Kit 2, 12, 38. In contrast, higher levels of c‐Kit protein are observed in healthy old individuals.…”

Section: Ischaemia/hypoxia‐associated Mirna Signatures In Atherosclermentioning

confidence: 98%

“…The opposite effects observed for the miR‐221 family in VSMCs have been related to different expression profiles of their target genes in two cell types, p27, p57 (anti‐proliferative) and c‐Kit (pro‐proliferative) 2, 40. The p27/p57 versus c‐Kit is highly expressed in VSMCs, while c‐Kit versus p27/p57 is highly expressed in ECs.…”

Section: Ischaemia/hypoxia‐associated Mirna Signatures In Atherosclermentioning

confidence: 99%

“…The most shared miRNAs are endothelial cell (EC) derived and include miR‐126/17–92/15/34 clusters as representing highly circulating miRNAs 2, 3, 4, 5, 6.…”

Section: Differentially Expressed Mirnas Act As Switchers or Fine‐tunersmentioning

confidence: 99%

“…The miR‐126 control vascular inflammation by regulating the expression of adhesion molecules requiring for leucocyte adherence to ECs, such as VCAM‐1 2.…”

Section: Mirna Signatures Related To Pathological Inflammatory Conditmentioning

confidence: 99%

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MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

Pourrajab

Zarch

Hekmatimoghaddam

et al. 2015

J Cellular Molecular Medi

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The age‐related senescence of adult tissues is associated with the decreased level of angiogenic capability and with the development of a degenerative disease such as atherosclerosis which thereafter result in the deteriorating function of multiple systems. Findings indicate that tissue senescence not only diminishes repair processes but also promotes atherogenesis, serving as a double‐edged sword in the development and prognosis of ischaemia‐associated diseases. Evidence evokes microRNAs (miRNAs) as molecular switchers that underlie cellular events in different tissues. Here, miRNAs would promote new potential targets for optimizing therapeutic methods in blood flow recovery to the ischaemic area. Effectively beginning an ischaemia therapy, a more characteristic of miRNA changes in adult tissues is prerequisite and in the forefront. It may also be a preliminary phase in treatment strategies by stem cell‐based therapy.

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Section: Ischaemia/hypoxia‐associated Mirna Signatures In Atherosclermentioning

confidence: 98%

Section: Ischaemia/hypoxia‐associated Mirna Signatures In Atherosclermentioning

confidence: 99%

“…The most shared miRNAs are endothelial cell (EC) derived and include miR‐126/17–92/15/34 clusters as representing highly circulating miRNAs 2, 3, 4, 5, 6.…”

Section: Differentially Expressed Mirnas Act As Switchers or Fine‐tunersmentioning

confidence: 99%

“…The miR‐126 control vascular inflammation by regulating the expression of adhesion molecules requiring for leucocyte adherence to ECs, such as VCAM‐1 2.…”

Section: Mirna Signatures Related To Pathological Inflammatory Conditmentioning

confidence: 99%

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MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

Pourrajab

Zarch

Hekmatimoghaddam

et al. 2015

J Cellular Molecular Medi

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“…According to crosslinking, ligation, and sequencing of hybrids (CLASH), it was discovered that two Other findings of angiogenesis inhibition by miR-221 in HUVECs 60,94,95) could demonstrate how it is difficult to extrapolate data about miR-221 in different tissues. Recently, by an in silico analysis, we found miR-221 to have a role in the advanced stages of atherosclerosis 96) .…”

Section: -2 Cxcl16 and Micrornamentioning

confidence: 99%

CXCL16 in Vascular Pathology Research: from Macro Effects to microRNAs

Jovanović

Živković

Djurić

et al. 2015

J Atheroscler Thromb

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Chemokines and their receptors have become significant factors in atherosclerosis research. CXCL16 is a multifunctional agent located on a separate locus to all other known chemokines and binds only to its "unique" receptor named CXCR6. As a scavenger receptor, adhesion molecule, and chemokine, it quickly became an interesting target in atherosclerosis research as all its functions have a role in vascular pathology. The investigation of the role of CXCL16 in atherosclerosis, although shown in in vitro studies, animal knockout models, and CXCL16 gene polymorphisms, haplotypes, and circulating levels, still shows puzzling results. Genetic and epigenetic studies have just scratched the surface of research necessary for a better assessment of the significance and perspective of this marker in plaque development and progression. In this review, we will summarize current knowledge about CXCL16 in atherosclerosis. Additionally, we will point out the importance of bioinformatics tools for the detection of potentially new CXCL16 regulatory networks through microRNA activity. This review aims to provide a better understanding of the underlying mechanisms, define more specific biomarkers, and discover new therapeutic targets.

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Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

643

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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Role of microRNAs in endothelial inflammation and senescence

Cited by 86 publications

References 82 publications

MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

CXCL16 in Vascular Pathology Research: from Macro Effects to microRNAs

Ischemia/Reperfusion

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