MicroRNA-34a regulates cardiac fibrosis after myocardial infarction by targeting Smad4

Huang, Ying; Yuan, Quan; Du, Jian-qing; Dai-fu, Zhang

doi:10.1517/14728222.2014.961424

Cited by 95 publications

(93 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…By directly targeting Smad4, miR-34a plays a key role in the progression of cardiac fibrosis. These findings suggest that miR-34a may be a new marker for cardiac fibrosis [35].…”

Section: Micrornasmentioning

confidence: 80%

Biomarkers in patients with myocardial fibrosis

Yang

Zheng

et al. 2017

Open Life Sciences

View full text Add to dashboard Cite

show abstract

“…By directly targeting Smad4, miR-34a plays a key role in the progression of cardiac fibrosis. These findings suggest that miR-34a may be a new marker for cardiac fibrosis [35].…”

Section: Micrornasmentioning

confidence: 80%

Biomarkers in patients with myocardial fibrosis

Yang

Zheng

et al. 2017

Open Life Sciences

View full text Add to dashboard Cite

show abstract

“…39, 41 Several other studies have also shown that SMAD4 is a target of miR-34a in functional studies involving solid tumor cell lines. 40,56 Further studies are needed to elucidate the exact roles that miR-34a might play in CLL in TP53-dependent and independent settings; and in ibrutinib-induced cell growth inhibition and cell death.…”

Section: Discussionmentioning

confidence: 99%

Ibrutinib downregulates a subset of miRNA leading to upregulation of tumor suppressors and inhibition of cell proliferation in chronic lymphocytic leukemia

et al. 2016

View full text Add to dashboard Cite

The lymph node (LN) is the site of chronic lymphocytic leukemia (CLL) cell activation and proliferation. Aberrant microRNA (miRNA) expression has been shown to have a role in CLL pathogenesis; however, a comparison of miRNA expression between CLL cells in the LN and the peripheral blood (PB) has previously not been reported. On the basis of the analysis of 17 paired LN and PB samples from CLL patients, we identify a panel of miRNAs that are increased in LN CLL cells correlating with an activation phenotype. When evaluated in CLL cells from 38 patients pre and post treatment with ibrutinib, a subset of these miRNAs (miR-22, miR-34a, miR-146b and miR-181b) was significantly decreased in response to ibrutinib. A concomitant increase in putative miRNA target transcripts (ARID1B, ARID2, ATM, CYLD, FOXP1, HDAC1, IBTK, PTEN and SMAD4) was also observed. Functional studies confirmed targets of ibrutinib-responsive miRNAs to include messenger RNA transcripts of multiple tumor suppressors. Knockdown of endogenous miR-34a and miR146b resulted in increased transcription of tumor suppressors and inhibition of cell proliferation. These findings demonstrate that ibrutinib downregulates the expression of a subset of miRNAs related to B-cell activation leading to increased expression of miRNA targets including tumor suppressors and a reduction in cell proliferation.

show abstract

“…Lawrie et al found the miRNA in the human serum in 2008 [20] . Since then, a great number of researches have explained that the miRNA in the circulating blood could stably exist in the extracellular fluids such as serum and plasma [21,22]. miR-208a is the cardiac-specific miRNA, which can regulate the physiological and pathological process of generation, development and damage repair; and its content is stable in the blood [23][24][25][26] .…”

Section: Discussionmentioning

confidence: 99%