Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

10.9K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.9K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

3.9K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.9K
Introduction to Fibroblasts01:09

Introduction to Fibroblasts

4.3K
Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
4.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effectiveness of Chemotherapy With/Without Radiotherapy for Locally Advanced Esophageal Squamous Cell Carcinoma: A Population-based Target Trial Emulation Study.

Anticancer research·2026
Same author

Effect of PM2.5 exposure on the risk of incident autoimmune diseases: a prospective cohort study in Taiwan.

Archives of public health = Archives belges de sante publique·2026
Same author

Development of a dual-energy CBCT calibration method for accurate electron density estimation in preclinical small-animal proton therapy dose planning.

Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine·2026
Same author

Unveiling mechanistic insights of inactivated Aspergillus niger spore by fishery-waste-derived chitosan via synchrotron radiation tomography.

Carbohydrate polymers·2026
Same author

2026 Consensus and review of Lipoprotein(a) from Taiwan Society of Lipid and Atherosclerosis: Molecular pathogenesis, epidemiology, clinical implications, and advances in diagnostic strategies.

Journal of the Formosan Medical Association = Taiwan yi zhi·2026
Same author

Association of atrial high-rate episodes daily burden with the risk of cardiovascular death, heart failure hospitalization, and stroke.

Heart rhythm·2026

Related Experiment Video

Updated: Mar 28, 2026

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
04:37

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis

Published on: April 25, 2025

1.8K

FTO modulates fibrogenic responses in obstructive nephropathy.

Chao-Yung Wang1, Shian-Sen Shie2, Ming-Lung Tsai1

  • 1Department of Cardiology, Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taiwan.

Scientific Reports
|January 5, 2016
PubMed
Summary

The fat mass and obesity-associated (FTO) gene is crucial in kidney fibrosis. FTO deficiency reduces fibrogenic responses, suggesting therapeutic potential for chronic kidney disease.

More Related Videos

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

2.3K
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

Related Experiment Videos

Last Updated: Mar 28, 2026

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
04:37

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis

Published on: April 25, 2025

1.8K
Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

2.3K
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

Area of Science:

  • Nephrology
  • Genetics
  • Molecular Biology

Background:

  • Genome-wide association studies link fat mass and obesity-associated (FTO) gene variants to body mass index, obesity, and chronic kidney disease outcomes.
  • The specific role of FTO within the kidney remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function of FTO in the context of kidney injury and fibrosis.

Main Methods:

  • Examined FTO expression levels in kidneys following ureteral obstruction.
  • Assessed the impact of FTO deficiency on renal fibrotic responses in a mouse model.
  • Analyzed the production of alpha-smooth muscle actin (α-SMA) in renal tubular cells stimulated with TGF-β.
  • Performed global gene transcription analysis in FTO-deficient kidneys post-obstruction.

Main Results:

  • FTO expression significantly increases after ureteral obstruction and in fibrotic kidneys.
  • FTO gene deficiency markedly reduces the kidney's fibrogenic response to ureteral obstruction.
  • Renal tubular cells lacking FTO exhibit decreased α-SMA production upon TGF-β stimulation.
  • FTO is essential for extracellular matrix synthesis in obstructed kidneys, with reduced gene transcription amplitude in FTO-deficient kidneys.

Conclusions:

  • FTO plays a critical role in the development of renal fibrosis.
  • Targeting FTO may offer a novel therapeutic strategy for kidney fibrosis and chronic kidney disease.