PMID- 31474862
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 10
DP  - 2019
TI  - microRNA Crosstalk Influences Epithelial-to-Mesenchymal, 
      Endothelial-to-Mesenchymal, and Macrophage-to-Mesenchymal Transitions in the 
      Kidney.
PG  - 904
LID - 10.3389/fphar.2019.00904 [doi]
LID - 904
AB  - microRNAs (miRNAs) are small, non-coding nucleotides that regulate diverse 
      biological processes. Altered microRNA biosynthesis or regulation contributes to 
      pathological processes including kidney fibrosis. Kidney fibrosis is 
      characterized by deposition of excess extracellular matrix (ECM), which is caused 
      by infiltration of immune cells, inflammatory cells, altered chemokines, and 
      cytokines as well as activation and accumulation of fibroblasts in the kidney. 
      These activated fibroblasts can arise from epithelial cells via 
      epithelial-to-mesenchymal transition (EMT), from bone marrow-derived M2 phenotype 
      macrophages via macrophage-to-mesenchymal transition (MMT), from endothelial 
      cells via endothelial-to-mesenchymal transition (EndMT), from resident 
      fibroblasts, and from bone marrow-derived monocytes and play a crucial role in 
      fibrotic events. Disrupted microRNA biosynthesis and aberrant regulation 
      contribute to the activation of mesenchymal programs in the kidney. miR-29 
      regulates the interaction between dipeptidyl peptidase-4 (DPP-4) and integrin beta1 
      and the associated active transforming growth factor beta (TGFbeta) and pro-EndMT 
      signaling; however, miR-let-7 targets transforming growth factor beta receptors 
      (TGFbetaRs) to inhibit TGFbeta signaling. N-acetyl-seryl-aspartyl-lysyl-proline 
      (AcSDKP) is an endogenous anti-fibrotic peptide, which is associated with 
      fibroblast growth factor receptor 1 (FGFR1) phosphorylation and subsequently 
      responsible for the production of miR-let-7. miR-29 and miR-let-7 family clusters 
      participate in crosstalk mechanisms, which are crucial for endothelial cell 
      homeostasis. The physiological level of AcSDKP is vital for the activation of 
      anti-fibrotic mechanisms including restoration of anti-fibrotic microRNA 
      crosstalk and suppression of profibrotic signaling by mitigating DPP-4-associated 
      mesenchymal activation in the epithelial cells, endothelial cells, and M2 
      phenotype macrophages. The present review highlights recent advancements in the 
      understanding of both the role of microRNAs in the development of kidney disease 
      and their potential as novel therapeutic targets for fibrotic disease states.
FAU - Srivastava, Swayam Prakash
AU  - Srivastava SP
AD  - Department of Pediatrics, Yale University School of Medicine, New Haven, CT, 
      United States.
FAU - Hedayat, Ahmad Fahim
AU  - Hedayat AF
AD  - Department of Pediatrics, Yale University School of Medicine, New Haven, CT, 
      United States.
FAU - Kanasaki, Keizo
AU  - Kanasaki K
AD  - Internal Medicine 1, Shimane University Faculty of Medicine, Izumo, Japan.
FAU - Goodwin, Julie E
AU  - Goodwin JE
AD  - Department of Pediatrics, Yale University School of Medicine, New Haven, CT, 
      United States.
LA  - eng
GR  - R01 HL131952/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20190816
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
EIN - Front Pharmacol. 2020 Jan 10;11:11. PMID: 31998136
PMC - PMC6707424
OTO - NOTNLM
OT  - diabetic kidney disease
OT  - endothelial-to-mesenchymal transition
OT  - epithelial-to-mesenchymal transition
OT  - kidney fibrosis
OT  - macrophage-to-mesenchymal transition
OT  - microRNA crosstalk
OT  - microRNAs
EDAT- 2019/09/03 06:00
MHDA- 2019/09/03 06:01
PMCR- 2019/08/16
CRDT- 2019/09/03 06:00
PHST- 2019/01/25 00:00 [received]
PHST- 2019/07/18 00:00 [accepted]
PHST- 2019/09/03 06:00 [entrez]
PHST- 2019/09/03 06:00 [pubmed]
PHST- 2019/09/03 06:01 [medline]
PHST- 2019/08/16 00:00 [pmc-release]
AID - 10.3389/fphar.2019.00904 [doi]
PST - epublish
SO  - Front Pharmacol. 2019 Aug 16;10:904. doi: 10.3389/fphar.2019.00904. eCollection 
      2019.