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Review
. 2010 Mar 2;121(8):1022-32.
doi: 10.1161/CIRCULATIONAHA.109.889048.

MicroRNAs add a new dimension to cardiovascular disease

Affiliations
Review

MicroRNAs add a new dimension to cardiovascular disease

Eric M Small et al. Circulation. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest Disclosures Eric M. Small: None; Robert J.A. Frost: None; Eric N. Olson: Co-founder of Miragen Therapeutics.

Figures

Figure 1
Figure 1
Regulated miRNAs in cardiovascular disease. Disease state is listed in top row and the particular study for each column is stated below. Heat map illustrates level of up-or down-regulation based on color scheme in legend. All miRNAs that were similarly regulated in at least two independent studies are listed to the left of the heat map. The last column lists the most abundant cardiac miRNAs in order of expression level in mice, which might be slightly different from the expression in humans. miRNAs with the same seed region (nucleotides 2-8) were combined into families due to putatively similar functions and due to technical difficulties in distinguishing very similar miRNAs with micro-arrays, northern-blotting or real-time PCR. The family was labeled as regulated if at least one member was changed. Let-7 family, let-7b,c,d,e,f,g,h,i,j; miR-15 family, miR-15a,b/16/195/424/497, miR-29 family, miR-29a,b,c; miR-30 family, miR-30a,b,c,d,e; miR-17 family, miR-17-5p/20a,b/93/106a,b. TAC, thoracic aortic constriction; MI, myocardial infarction; BZ, border zone; RM, remote myocardium; HF, heart failure; DCM, dilated cardiomyopathy; ICM, ischemic cardiomyopathy; AS, aortic stenosis; CAA, carotid artery angioplasty.
Figure 2
Figure 2
Published target mRNAs and functional role of disease related microRNAs in cardiomyocytes and fibroblasts. Targets that could not be validated in later publications are labeled with a (?). The arrow adjacent to miRNA illustrates whether the miRNA is up or downregulated in cardiac disease. Green and purple shaded regions indicate stimulation or repression of a process in cardiac disease, respectively. AP-1, activator protein 1; CDC42, cell division cycle 42; CTGF, connective tissue growth factor; Cx43, connexin 43; Hand2, heart and neural crest derivatives expressed 2; HCN2, hyperpolarization activated cyclic nucleotide-gated potassium channel 2; HIF1α, Hypoxia inducible factor; Hop, homeodomain-only protein; Hsp, heat shock protein; Irx5, Iroquois homeobox protein 5; Kcnd2, potassium voltage-gated channel subfamily D member 2; Kcnj2, potassium inwardly-rectifying channel, subfamily J, member 2; MEF2, myocyte enhancing factor-2; MuRF 1, muscle RING-finger protein 1; PDCD4, programmed cell death 4; PHD2, prolyl hydroxylase 2; PP2A, B56a regulatory subunit of protein phosphatase 2a; PTEN, phosphatase and tissue homolog; RhoA, Ras homolog gene family, member A; Sirt1, Sirtuin; SRF, serum response factor; Thrap1, thyroid hormone receptor associated protein1
Figure 3
Figure 3
Published target mRNAs and functional role of disease related miRNAs in vascular remodeling and angiogenesis. Spindle shaped yellow cells represent vascular smooth muscle cells (SMCs) and cuboidal grey cells represent endothelial cells (ECs). Purple and green shaded regions indicate microRNAs with “pro-angiogenic” and “anti-angiogenic” characteristics, respectively. ACE, angiotensin converting enzyme; SuFu, suppressor of fused; Shh, sonic hedgehog; HGS, Hepatocyte growth factor-regulated tyrosine kinase substrate; IGF, insulin-like growth factor; ITGA5, integrin-α5; PIK3R2, phosphoinositol-3 kinase regulatory subunit 2 (p85β); PTEN, phosphatase and tensin homolog; Spred-1, sprouty-related EVH domain-containing protein-1; VCAM-1, vascular cell adhesion molecule.

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