4.5 Article

An emerging role for the miR-26 family in cardiovascular disease

期刊

TRENDS IN CARDIOVASCULAR MEDICINE
卷 24, 期 6, 页码 241-248

出版社

ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2014.06.003

关键词

-

资金

  1. National Institutes of Health, USA [HL091076, HL115141, HL117994]
  2. Institutional Ruth L. Kirschstein N.R.S.A. [T32HL07604]
  3. Jonathan A. Levy Research Award

向作者/读者索取更多资源

In response to acute myocardial infarction (MI), a complex series of cellular and molecular signaling events orchestrate the myocardial remodeling that ensues weeks to months after injury. Clinical, epidemiological, and pathological studies demonstrate that inadequate or impaired angiogenesis after myocardial injury is often associated with decreased left ventricular (LV) function and clinical outcomes. The microRNA family, miR-26, plays diverse roles in regulating key aspects of cellular growth, development, and activation. Recent evidence supports a central role for the miR-26 family in cardiovascular disease by controlling critical signaling pathways, such as BMP/SMAD1 signaling, and targets relevant to endothelial cell growth, angiogenesis, and LV function post-MI. Emerging studies of the miR-26 family in other cell types including vascular smooth muscle cells, cardiac fibroblasts, and cardiomyocytes suggest that miR-26 may bear important implications for a range of cardiovascular repair mechanisms. This review examines the current knowledge of the miR-26 family's role in key cell types that critically control cardiovascular disease under pathological and physiological stimuli. (C) 2014 Elsevier Inc. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Article Biology

Methotrexate attenuates vascular inflammation through an adenosine-microRNA-dependent pathway

Dafeng Yang, Stefan Haemmig, Haoyang Zhou, Daniel Perez-Cremades, Xinghui Sun, Lei Chen, Jie Li, Jorge Haneo-Mejia, Tianlun Yang, Ivana Hollan, Mark W. Feinberg

Summary: The study shows that MTX and its metabolite adenosine exert anti-inflammatory effects in vascular endothelium by targeting and activating Mir181b expression. Specifically, MTX can attenuate inflammation and EC activation in a Mir181a2b2-dependent manner, indicating a potential therapeutic opportunity for anti-inflammatory therapy.
Article Chemistry, Multidisciplinary

MicroRNA-17-3p suppresses NF-κB-mediated endothelial inflammation by targeting NIK and IKKβ binding protein

Yin Cai, Yu Zhang, Hui Chen, Xing-hui Sun, Peng Zhang, Lu Zhang, Meng-yang Liao, Fang Zhang, Zheng-yuan Xia, Ricky Ying-keung Man, Mark W. Feinberg, Susan Wai-Sum Leung

Summary: miR-17-3p inhibits LPS-induced NF-kappa B activation by targeting NIBP, thereby effectively suppressing pro-inflammatory responses in vascular endothelium.

ACTA PHARMACOLOGICA SINICA (2021)

Article Hematology

Novel Lesional Transcriptional Signature Separates Atherosclerosis With and Without Diabetes in Yorkshire Swine and Humans

Stefan Haemmig, Ali Hashemi Gheinani, Marina Zaromytidou, Gerasimos Siasos, Ahmet Umit Coskun, Michelle A. Cormier, David A. Gross, A. K. M. Khyrul Wara, Antonios P. Antoniadis, Xinghui Sun, Galina K. Sukhova, Fred G. P. Welt, Ioannis Andreou, Carl Whatling, Li-Ming Gan, Johannes Wikstrom, Elazer R. Edelman, Peter Libby, Peter H. Stone, Mark W. Feinberg

Summary: This study identified evolutionarily conserved gene signatures and signaling pathways that distinguish diabetes-related and non-diabetes-related atherosclerosis. By utilizing genome-wide transcriptomics, the research successfully differentiated between atherosclerosis associated with diabetes and that not associated with diabetes, providing new insights and therapeutic opportunities.

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY (2021)

Article Hematology

Gene Expression Signature in Patients With Symptomatic Peripheral Artery Disease

Jonathan D. Newman, MacIntosh G. Cornwell, Hua Zhou, Caron Rockman, Adriana Heguy, Yajaira Suarez, Henry S. Cheng, Mark W. Feinberg, Judith S. Hochman, Kelly Ruggles, Jeffrey S. Berger

Summary: A transcriptomic signature identified patients with symptomatic PAD and those at increased risk of major adverse cardiac or limb events (MACLE). A specific microRNA, microRNA-4477b, was found to be overexpressed in prevalent PAD, incident MACLE, and in a mouse hindlimb ischemia model. This novel signature provides insights into potential mechanisms of severe symptomatic PAD.

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY (2021)

Article Biochemistry & Molecular Biology

MiR-409-3p targets a MAP4K3-ZEB1-PLGF signaling axis and controls brown adipose tissue angiogenesis and insulin resistance

Dakota Becker-Greene, Hao Li, Daniel Perez-Cremades, Winona Wu, Furkan Bestepe, Denizhan Ozdemir, Carolyn E. Niosi, Ceren Aydogan, Dennis P. Orgill, Mark W. Feinberg, Basak Icli

Summary: The study identified miR-409-3p as a critical regulator of EC-BAT crosstalk by modulating a ZEB1-MAP4K3-PLGF signaling axis, resulting in improved BAT angiogenesis, glucose tolerance, and energy expenditure in mice with diet-induced obesity.

CELLULAR AND MOLECULAR LIFE SCIENCES (2021)

Article Cardiac & Cardiovascular Systems

MicroRNA-mediated control of myocardial infarction in diabetes

Daniel Perez-Cremades, Jingshu Chen, Carmel Assa, Mark W. Feinberg

Summary: Diabetes mellitus is a global public health problem that is expected to continue increasing due to the rise in obesity and aging population. Individuals with diabetes have a higher risk of cardiovascular complications, particularly myocardial infarction (MI). In the past two decades, studies have revealed the role of stage-specific miRNAs in the hearts of people with diabetes and MI, impacting cardiomyocyte death, angiogenesis, inflammatory response, myocardial remodeling, and myocardial lipotoxicity. Understanding the significance of these miRNAs and their targets may lead to novel RNA-based therapeutic interventions for managing the increased risk of MI in diabetes.

TRENDS IN CARDIOVASCULAR MEDICINE (2023)

Article Medicine, Research & Experimental

Deficiency of lncRNA SNHG12 impairs ischemic limb neovascularization by altering an endothelial cell cycle pathway

David A. Gross, Henry S. Cheng, Rulin Zhuang, Michael G. McCoy, Daniel Perez-Cremades, Zachary Salyers, A. K. M. Khyrul Wara, Stefan Haemmig, Terence E. Ryan, Mark W. Feinberg

Summary: SNHG12 is a dysregulated long noncoding RNA (lncRNA) in atherosclerosis, and it plays a significant role in the regulation of vascular senescence and angiogenic response. The deficiency of SNHG12 reduces cell proliferation, migration, and endothelial sprouting, while overexpression promotes these angiogenic functions. SNHG12 may exert its effects through interacting with proteins like IGF2BP3, and it is involved in cell cycle regulation and signaling pathways related to Wnt, Notch, and angiopoietin signaling pathways.

JCI INSIGHT (2022)

Article Cardiac & Cardiovascular Systems

Isolation and culture of murine aortic cells and RNA isolation of aortic intima and media: Rapid and optimized approaches for atherosclerosis research

Jingshu Chen, Rulin Zhuang, Henry S. Cheng, Anurag Jamaiyar, Carmel Assa, Michael McCoy, Shruti Rawal, Daniel Perez-Cremades, Mark W. Feinberg

Summary: A new method for isolating and culturing diverse cell types from the mouse aorta simultaneously has been developed, allowing for the extraction of highly pure cells for studying the function and mechanisms of various vascular diseases.

ATHEROSCLEROSIS (2022)

Article Cardiac & Cardiovascular Systems

Endothelial cell-specific deletion of a microRNA accelerates atherosclerosis

Dafeng Yang, Stefan Haemmig, Jingshu Chen, Michael McCoy, Henry S. Cheng, Haoyang Zhou, Xiao Cheng, Xinghui Sun, Jorge Haneo-Mejia, Shamsudheen K. Vellarikkal, Rajat M. Gupta, Victor Barrera, Mark W. Feinberg

Summary: In this study, the researchers investigated the role of miRNA deficiency in vascular endothelial cells during atherogenesis using a mouse model. They found that the specific deletion of miR-181a2b2 in endothelial cells promoted atherosclerotic lesion formation, cell adhesion molecule expression, and the influx of macrophages in the vessel wall. However, the deletion of miR-181a2b2 did not affect body weight, lipid metabolism, or inflammation levels in circulating peripheral blood mononuclear cells. The study suggests that miR-181a2b2 deficiency in endothelial cells plays a crucial role in regulating key pathways involved in endothelial inflammation and atherosclerosis development.

ATHEROSCLEROSIS (2022)

Article Cardiac & Cardiovascular Systems

Perivascular Fibrosis Is Mediated by a KLF10-IL-9 Signaling Axis in CD4+T Cells

Rulin Zhuang, Jingshu Chen, Henry S. Cheng, Carmel Assa, Anurag Jamaiyar, Arvind K. Pandey, Daniel Perez-Cremades, Bofang Zhang, Aspasia Tzani, Akm Khyrul Wara, Jorge Plutzky, Victor Barrera, Preetida Bhetariya, Richard N. Mitchell, Zhongmin Liu, Mark W. Feinberg

Summary: Transcription factor KLF10 is upregulated in CD4+ T cells of hypertensive individuals and Ang II-treated mice. Deficiency of Klf10 exacerbates perivascular fibrosis and multi-organ dysfunction in response to Ang II. Klf10 or IL-9 may represent novel therapeutic targets for the treatment of vascular or fibrotic diseases.

CIRCULATION RESEARCH (2022)

Article Biochemistry & Molecular Biology

A miRNA cassette reprograms smooth muscle cells into endothelial cells

Michael G. McCoy, Daniel Perez-Cremades, Nathan Belkin, Wenhui Peng, Bofang Zhang, Jingshu Chen, Madhur Sachan, A. K. M. Khyrul Wara, Rulin Zhuang, Henry S. Cheng, Mark W. Feinberg

Summary: This study demonstrates that a 4-miRNA cassette can reprogram vascular smooth muscle cells into endothelial cells, and these induced cells exhibit high similarity to native endothelial cells. Injected induced cells even restore blood flow faster than conventional endothelial cells in a mouse model, suggesting the potential of this approach for vascular disease therapy.

FASEB JOURNAL (2022)

Article Biochemistry & Molecular Biology

miR-181b regulates vascular endothelial aging by modulating an MAP3K3 signaling pathway

Haoyang Zhou, Dafeng Yang, Henry S. Cheng, Michael G. McCoy, Daniel Perez-Cremades, Stefan Haemmig, Danny Wong, Lei Chen, Mark W. Feinberg

Summary: The study uncovers an important role of miR-181b in regulating vascular endothelial aging through the MAP3K3-MAPK signaling pathway, revealing potential therapeutic targets for anti-aging therapy in cardiovascular disease.

FASEB JOURNAL (2022)

Article Multidisciplinary Sciences

Antirheumatic therapy is associated with reduced complement activation in rheumatoid arthritis

Thao H. P. Nguyen, Ingrid Hokstad, Morten Wang Fagerland, Tom Eirik Mollnes, Ivana Hollan, Mark W. Feinberg, Gunnbjorg Hjeltnes, Gro O. Eilertsen, Knut Mikkelsen, Stefan Agewall

Summary: This study found that patients with active RA had elevated levels of complement activation, and TCC levels decreased after anti-rheumatic treatment within 6 weeks, but only TNFi +/- MTX treatment led to sustained reduction in TCC during the 6-month follow-up period. RA patients with endothelial dysfunction had higher baseline TCC compared to those without, indicating the potential involvement of complement in the atherosclerotic process in RA.

PLOS ONE (2022)

Article Peripheral Vascular Disease

MicroRNA-375 repression of Kruppel-like factor 5 improves angiogenesis in diabetic critical limb ischemia

Michael G. McCoy, Anurag Jamaiyar, Grasiele Sausen, Henry S. Cheng, Daniel Perez-Cremades, Rulin Zhuang, Jingshu Chen, Philip P. Goodney, Mark A. Creager, Marc S. Sabatine, Marc P. Bonaca, Mark W. Feinberg

Summary: Peripheral artery disease (PAD) is a serious condition that can lead to limb loss and death, especially in subjects with diabetes. In this study, researchers identified miR-375 as a potential therapeutic target for critical limb ischemia (CLI), an advanced form of PAD. They found that miR-375, when overexpressed, promotes angiogenesis and arteriogenesis, improving blood flow recovery in diabetic mice. Further investigation revealed that miR-375 regulates the NF-kB signaling pathway by targeting Kruppel-like factor 5 (KLF5). These findings suggest that targeting the miR-375-KLF5-NF-kB signaling axis may be an effective strategy for treating CLI in diabetes.

ANGIOGENESIS (2023)

Article Cardiac & Cardiovascular Systems

KLF10 deficiency in CD4+T cells promotes atherosclerosis progression by altering macrophage dynamics

Akm Khyrul Wara, Shruti Rawal, Xilan Yang, Daniel Perez-Cremades, Madhur Sachan, Jingshu Chen, Mark W. Feinberg

Summary: This study identifies a critical role for the transcription factor KLF10 in regulating the interactions between CD4+ Tregs and macrophages in atherosclerosis. Knockout of KLF10 in CD4+ T cells leads to exaggerated plaque progression due to defects in the immunosuppressive functions of Tregs on macrophages. Adoptive cellular therapy with WT Tregs reverses the accelerated lesion progression and deleterious effects in KLF10 knockout mice.

ATHEROSCLEROSIS (2022)

暂无数据