Hui Yao Lan

Summary

Affiliation: The Chinese University of Hong Kong
Country: China

Publications

  1. Wang Y, Jiang H, Pan J, Huang X, Wang Y, Huang H, et al. Macrophage-to-Myofibroblast Transition Contributes to Interstitial Fibrosis in Chronic Renal Allograft Injury. J Am Soc Nephrol. 2017;28:2053-2067 pubmed publisher
    ..Moreover, the transition of bone marrow-derived M2-type macrophages to myofibroblasts in the renal allograft is regulated via a Smad3-dependent mechanism. ..
  2. Fu S, Tang Y, Huang X, Feng M, Xu A, Lan H. Smad7 protects against acute kidney injury by rescuing tubular epithelial cells from the G1 cell cycle arrest. Clin Sci (Lond). 2017;131:1955-1969 pubmed publisher
    ..In conclusion, Smad7 plays a protective role in AKI. Blockade of TGF-β/Smad3-p21/p27-induced G1 cell cycle arrest may be a key mechanism by which Smad7 treatment inhibits AKI. Thus, Smad7 may be a novel therapeutic agent for AKI. ..
  3. Lan H. Transforming growth factor-β/Smad signalling in diabetic nephropathy. Clin Exp Pharmacol Physiol. 2012;39:731-8 pubmed publisher
    ..Targeting downstream TGF-β/Smad signalling by overexpressing Smad7- or Smad3-dependent microRNA related to fibrosis may represent a novel and effective strategy for the treatment of DN. ..
  4. Lai W, Tang Y, Huang X, Ming Kuen Tang P, Xu A, Szalai A, et al. C-reactive protein promotes acute kidney injury via Smad3-dependent inhibition of CDK2/cyclin E. Kidney Int. 2016;90:610-26 pubmed publisher
    ..Thus, C-reactive protein may promote AKI by impairing tubular epithelial cell regeneration via the CD32-Smad3-p27-driven inhibition of the CDK2/cyclin E complex. Targeting Smad3 may offer a new treatment approach for AKI. ..
  5. Liu Z, Huang X, Chen H, Fung E, Liu J, Lan H. Deletion of Angiotensin-Converting Enzyme-2 Promotes Hypertensive Nephropathy by Targeting Smad7 for Ubiquitin Degradation. Hypertension. 2017;70:822-830 pubmed publisher
    ..Overexpression of renal Smad7 protects against hypertensive nephropathy by inactivating angiotensin II-induced TGF-β/Smad3 and NF-κB pathways and by targeting the Smad3-dependent microRNA-21 axis. ..
  6. Tang P, Zhou S, Li C, Liao J, Xiao J, Wang Q, et al. The proto-oncogene tyrosine protein kinase Src is essential for macrophage-myofibroblast transition during renal scarring. Kidney Int. 2018;93:173-187 pubmed publisher
    ..Thus, macrophage-myofibroblast transition contributes to Src-mediated tissue fibrosis. Hence, targeting Src may represent as a precision therapeutic strategy for macrophage-myofibroblast transition-driven fibrotic diseases. ..
  7. Sun S, Tang P, Feng M, Jun X, Huang X, Li P, et al. Novel lncRNA Erbb4-IR Promotes Diabetic Kidney Injury in db/db Mice by Targeting miR-29b. Diabetes. 2017;: pubmed publisher
    ..Targeting Erbb4-IR may represent a novel therapy for T2DN...
  8. Lan H, Chung A. Transforming growth factor-β and Smads. Contrib Nephrol. 2011;170:75-82 pubmed publisher
    ..In conclusion, TGF-β/Smad signaling plays a critical role in DN. A better understanding of the role of TGF-β/Smad signaling in the development of DN should provide an effective therapeutic strategy to combat DN. ..
  9. Lv L, Tang P, Li C, You Y, Li J, Huang X, et al. The pattern recognition receptor, Mincle, is essential for maintaining the M1 macrophage phenotype in acute renal inflammation. Kidney Int. 2017;91:587-602 pubmed publisher
    ..Hence, targeting Mincle may be a novel therapy for acute kidney injury associated with M1 macrophages. ..
  10. Yang C, Huang X, Fung E, Liu H, Lan H. The Regulatory T-cell Transcription Factor Foxp3 Protects against Crescentic Glomerulonephritis. Sci Rep. 2017;7:1481 pubmed publisher
    ..In conclusion, Foxp3 protects against kidney injury in crescentic GN through enhancement of Treg numbers and function, and suppression of Th1, Th2 and Th17 immune responses at the systemic and local tissue levels. ..

Locale

Detail Information

Publications15

  1. Wang Y, Jiang H, Pan J, Huang X, Wang Y, Huang H, et al. Macrophage-to-Myofibroblast Transition Contributes to Interstitial Fibrosis in Chronic Renal Allograft Injury. J Am Soc Nephrol. 2017;28:2053-2067 pubmed publisher
    ..Moreover, the transition of bone marrow-derived M2-type macrophages to myofibroblasts in the renal allograft is regulated via a Smad3-dependent mechanism. ..
  2. Fu S, Tang Y, Huang X, Feng M, Xu A, Lan H. Smad7 protects against acute kidney injury by rescuing tubular epithelial cells from the G1 cell cycle arrest. Clin Sci (Lond). 2017;131:1955-1969 pubmed publisher
    ..In conclusion, Smad7 plays a protective role in AKI. Blockade of TGF-β/Smad3-p21/p27-induced G1 cell cycle arrest may be a key mechanism by which Smad7 treatment inhibits AKI. Thus, Smad7 may be a novel therapeutic agent for AKI. ..
  3. Lan H. Transforming growth factor-β/Smad signalling in diabetic nephropathy. Clin Exp Pharmacol Physiol. 2012;39:731-8 pubmed publisher
    ..Targeting downstream TGF-β/Smad signalling by overexpressing Smad7- or Smad3-dependent microRNA related to fibrosis may represent a novel and effective strategy for the treatment of DN. ..
  4. Lai W, Tang Y, Huang X, Ming Kuen Tang P, Xu A, Szalai A, et al. C-reactive protein promotes acute kidney injury via Smad3-dependent inhibition of CDK2/cyclin E. Kidney Int. 2016;90:610-26 pubmed publisher
    ..Thus, C-reactive protein may promote AKI by impairing tubular epithelial cell regeneration via the CD32-Smad3-p27-driven inhibition of the CDK2/cyclin E complex. Targeting Smad3 may offer a new treatment approach for AKI. ..
  5. Liu Z, Huang X, Chen H, Fung E, Liu J, Lan H. Deletion of Angiotensin-Converting Enzyme-2 Promotes Hypertensive Nephropathy by Targeting Smad7 for Ubiquitin Degradation. Hypertension. 2017;70:822-830 pubmed publisher
    ..Overexpression of renal Smad7 protects against hypertensive nephropathy by inactivating angiotensin II-induced TGF-β/Smad3 and NF-κB pathways and by targeting the Smad3-dependent microRNA-21 axis. ..
  6. Tang P, Zhou S, Li C, Liao J, Xiao J, Wang Q, et al. The proto-oncogene tyrosine protein kinase Src is essential for macrophage-myofibroblast transition during renal scarring. Kidney Int. 2018;93:173-187 pubmed publisher
    ..Thus, macrophage-myofibroblast transition contributes to Src-mediated tissue fibrosis. Hence, targeting Src may represent as a precision therapeutic strategy for macrophage-myofibroblast transition-driven fibrotic diseases. ..
  7. Sun S, Tang P, Feng M, Jun X, Huang X, Li P, et al. Novel lncRNA Erbb4-IR Promotes Diabetic Kidney Injury in db/db Mice by Targeting miR-29b. Diabetes. 2017;: pubmed publisher
    ..Targeting Erbb4-IR may represent a novel therapy for T2DN...
  8. Lan H, Chung A. Transforming growth factor-β and Smads. Contrib Nephrol. 2011;170:75-82 pubmed publisher
    ..In conclusion, TGF-β/Smad signaling plays a critical role in DN. A better understanding of the role of TGF-β/Smad signaling in the development of DN should provide an effective therapeutic strategy to combat DN. ..
  9. Lv L, Tang P, Li C, You Y, Li J, Huang X, et al. The pattern recognition receptor, Mincle, is essential for maintaining the M1 macrophage phenotype in acute renal inflammation. Kidney Int. 2017;91:587-602 pubmed publisher
    ..Hence, targeting Mincle may be a novel therapy for acute kidney injury associated with M1 macrophages. ..
  10. Yang C, Huang X, Fung E, Liu H, Lan H. The Regulatory T-cell Transcription Factor Foxp3 Protects against Crescentic Glomerulonephritis. Sci Rep. 2017;7:1481 pubmed publisher
    ..In conclusion, Foxp3 protects against kidney injury in crescentic GN through enhancement of Treg numbers and function, and suppression of Th1, Th2 and Th17 immune responses at the systemic and local tissue levels. ..
  11. Lan H, Chung A. TGF-β/Smad signaling in kidney disease. Semin Nephrol. 2012;32:236-43 pubmed publisher
    ..Advances in understanding of the mechanisms of TGF-β/Smad signaling in renal fibrosis and inflammation during chronic kidney diseases should provide a better therapeutic strategy to combat kidney diseases. ..
  12. Zhou Q, Chung A, Huang X, Dong Y, Yu X, Lan H. Identification of novel long noncoding RNAs associated with TGF-β/Smad3-mediated renal inflammation and fibrosis by RNA sequencing. Am J Pathol. 2014;184:409-17 pubmed publisher
    ....
  13. Feng M, Tang P, Huang X, Sun S, You Y, Xiao J, et al. TGF-β Mediates Renal Fibrosis via the Smad3-Erbb4-IR Long Noncoding RNA Axis. Mol Ther. 2018;26:148-161 pubmed publisher
    ..Targeting Erbb4-IR may represent a precise therapeutic strategy for progressive renal fibrosis. ..
  14. Lan H. Diverse roles of TGF-β/Smads in renal fibrosis and inflammation. Int J Biol Sci. 2011;7:1056-67 pubmed
    ..Thus, targeting the downstream TGF-β/Smad3 signaling pathway by gene transfer of either Smad7 or Smad3-dependent microRNAs may represent a specific and effective therapeutic strategy for kidney disease. ..
  15. Tang Y, Chen J, Huang K, Luo D, Liang P, Feng M, et al. The incidence, risk factors and in-hospital mortality of acute kidney injury in patients after abdominal aortic aneurysm repair surgery. BMC Nephrol. 2017;18:184 pubmed publisher
    ....