BioMed Research International

Combating Kidney Fibrosis


Publishing date
05 Sep 2014
Status
Published
Submission deadline
18 Apr 2014

Lead Editor

1Department of Diabetology & Endocrinology, Kanazawa Medical University, Kahoku, Ishikawa, Japan

2Department of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan

3Department of Nephrology, Nizams Institute of Medical Sciences, Hyderabad, Andhrapradesh, India

4Renal Transplant Unit, Department of Nephrology and Renal Transplant, IDIBAPS-Barcelona University, Barcelona, Spain


Combating Kidney Fibrosis

Description

An estimated 10% of the world population has some form of kidney disease. Kidney fibrosis is the final common pathway of progressive kidney diseases, resulting in subsequent massive destruction of normal kidney structure and diminishing the function. The kidney fibrosis is caused by prolonged injury and dysregulation of normal wound healing process associated with an excessive abnormal extracellular matrix deposition. Kidney fibroblasts play a vital role, but the origin of fibroblasts remains to be under intensive discussion. Inflammatory cells and cytokines likely play an important role in fibroblast activation. Furthermore not only the fibroblast, but also any type of kidney cells can become extracellular matrix producing mesenchymal phonotypic cells. Apart from the different cells contributing in the fibrosis, there are many pathways, involved in the initiation and progression of kidney fibrosis. Currently approved therapies are neither pathway nor cell specific in nature, due to which these therapies became ineffective in reducing the fibrosis and are associated with side effects. The understanding of the pathways and cells which are involved in the fibrosis will guide the future therapies to combat the kidney fibrosis.

We invite investigators to contribute original research articles as well as review articles which will stimulate the continuing efforts to understand the molecular pathology underlying kidney fibrosis, the development of newer strategies to treat kidney fibrosis, tissue regeneration, and the evaluation of outcomes. We are particularly interested in articles describing the newer concepts in fibroblast activation process and inflammation and newer strategies in the area of kidney fibrosis and its therapy. Any kinds of disease models are welcome. Potential topics include, but are not limited to:

  • Clinical biomarkers
  • Advances in genetics/epigenetics
  • Newer concepts which can explain fibroblast activation process
  • Role of inflammation
  • Obstruction/stone leading to fibrosis
  • Role of cytokine/chemokines
  • Transplant kidney fibrosis
  • Diabetic kidney disease
  • Hypoxia in kidney fibrosis

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/bmri/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/pathology/ckf/ according to the following timetable:


Articles

  • Special Issue
  • - Volume 2014
  • - Article ID 679154
  • - Editorial

Combating Kidney Fibrosis

Keizo Kanasaki | Akito Maeshima | ... | Ignacio Revuelta
  • Special Issue
  • - Volume 2014
  • - Article ID 315494
  • - Review Article

Role of Nutrient-Sensing Signals in the Pathogenesis of Diabetic Nephropathy

Shinji Kume | Daisuke Koya | ... | Hiroshi Maegawa
  • Special Issue
  • - Volume 2014
  • - Article ID 124902
  • - Research Article

Effect of Angiotensin II and Small GTPase Ras Signaling Pathway Inhibition on Early Renal Changes in a Murine Model of Obstructive Nephropathy

Ana B. Rodríguez-Peña | Isabel Fuentes-Calvo | ... | José M. López-Novoa
  • Special Issue
  • - Volume 2014
  • - Article ID 837421
  • - Review Article

Hypoxia in Diabetic Kidneys

Yumi Takiyama | Masakazu Haneda
  • Special Issue
  • - Volume 2014
  • - Article ID 684765
  • - Research Article

The Proteasome Inhibitor, MG132, Attenuates Diabetic Nephropathy by Inhibiting SnoN Degradation In Vivo and In Vitro

Wei Huang | Chen Yang | ... | Yong Xu
  • Special Issue
  • - Volume 2014
  • - Article ID 324713
  • - Research Article

Wnt Pathway Activation in Long Term Remnant Rat Model

E. Banon-Maneus | J. Rovira | ... | J. M. Campistol
  • Special Issue
  • - Volume 2014
  • - Article ID 750602
  • - Review Article

The Interplay between Inflammation and Fibrosis in Kidney Transplantation

Irina B. Torres | Francesc Moreso | ... | Daniel Serón
  • Special Issue
  • - Volume 2014
  • - Article ID 782625
  • - Research Article

High Glucose Induces Sumoylation of Smad4 via SUMO2/3 in Mesangial Cells

Xueqin Zhou | Chenlin Gao | ... | Yong Xu
  • Special Issue
  • - Volume 2014
  • - Article ID 802841
  • - Research Article

Gremlin Activates the Smad Pathway Linked to Epithelial Mesenchymal Transdifferentiation in Cultured Tubular Epithelial Cells

Raquel Rodrigues-Diez | Raúl R. Rodrigues-Diez | ... | Marta Ruiz-Ortega
  • Special Issue
  • - Volume 2014
  • - Article ID 595493
  • - Review Article

Regenerative Medicine for the Kidney: Renotropic Factors, Renal Stem/Progenitor Cells, and Stem Cell Therapy

Akito Maeshima | Masao Nakasatomi | Yoshihisa Nojima
BioMed Research International
 Journal metrics
Acceptance rate31%
Submission to final decision67 days
Acceptance to publication30 days
CiteScore3.600
Impact Factor2.276
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