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

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

890
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
890
Stem Cell Niche01:26

Stem Cell Niche

6.2K
The stem cell niche is the dynamic microenvironment where stem cells reside. Inside these niches, the cells may remain undifferentiated, undergo high self-renewal, or become lineage-specific progenitors. Stem cells coexist with other niche cells, such as stromal cells. They also interact closely with the ECM. Cell-cell and cell-matrix communication occur via adhesion molecules or soluble factors that signal the stem cells and determine their fate. Stromal cells also provide survival signals to...
6.2K
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

572
Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
572
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

7.4K
The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
7.4K

You might also read

Related Articles

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

Sort by
Same author

Decade-Long Trends in Chronic Kidney Disease-Mineral and Bone Disorder Target Achievement and Mortality Associations among Chinese Hemodialysis Patients: Insights from the China DOPPS Study.

Kidney diseases (Basel, Switzerland)·2026
Same author

Fibrillin-1 Orchestrates a Pro-senescent Niche Driving Peritubular Endothelial Senescence via ZEB1/endothelin-1/β-catenin Signaling.

International journal of biological sciences·2026
Same author

Targeting fibrillin-1 disrupts the fibrogenic niche formation and ameliorates kidney fibrosis.

Journal of advanced research·2026
Same author

Obinutuzumab or Tacrolimus in Primary Membranous Nephropathy.

The New England journal of medicine·2026
Same author

Association and predictive value of biological aging for chronic kidney disease risk in diabetes: cross-cohort validation across the United Kingdom and China.

The journals of gerontology. Series A, Biological sciences and medical sciences·2026
Same author

Increased WNT10B/FOXO6 signaling promotes cell fate transition in renal tubular cells to aggravate renal inflammation and fibrosis.

Nature communications·2026

Related Experiment Video

Updated: Jan 16, 2026

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

2.2K

Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.

Li Li1,2, Jinlin Liao1,2, Yuxi Zhang1,2

  • 1State Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|October 3, 2025
PubMed
Summary

Tenascin C (TNC) creates a kidney fibrosis niche by activating macrophages via Toll-like receptor 4 (TLR4) signaling. Inhibiting TLR4 reduces kidney inflammation and fibrosis, offering a potential therapeutic target.

Keywords:
TNCfibrogenic nichekidney fibrosismacrophagessignal cell RNA sequencingspatial transcriptomics

More Related Videos

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

340
Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes
11:47

Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes

Published on: March 4, 2022

2.6K

Related Experiment Videos

Last Updated: Jan 16, 2026

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

2.2K
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

340
Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes
11:47

Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes

Published on: March 4, 2022

2.6K

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Kidney fibrosis, a common outcome of chronic kidney disease (CKD), originates from injury-induced fibrogenic niches.
  • Understanding the cellular and molecular mechanisms driving kidney fibrosis is crucial for developing effective treatments.

Purpose of the Study:

  • To delineate cellular heterogeneity, spatial organization, and molecular interactions within fibrotic kidney microenvironments.
  • To identify key molecular players orchestrating the development of renal inflammation and fibrosis.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) were employed on mouse kidneys subjected to ischemia-reperfusion injury.
  • Analysis of TNC-enriched microenvironments, macrophage activation pathways (TLR4/NF-κB), and therapeutic interventions (TLR4 inhibition/knockout).

Main Results:

  • A tenascin C (TNC)-enriched, proinflammatory, and profibrotic microenvironment was identified, promoting macrophage activation.
  • TNC and TNC-enriched scaffolds activated bone marrow-derived macrophages via Toll-like receptor 4 (TLR4)/NF-κB signaling.
  • Pharmacological inhibition or genetic knockout of TLR4 significantly alleviated renal inflammation and fibrosis by inhibiting macrophage activation.

Conclusions:

  • Tenascin C (TNC) plays a critical role in establishing a proinflammatory and profibrotic niche that drives kidney fibrosis.
  • Macrophage activation via the TLR4/NF-κB signaling pathway is a key mechanism in TNC-mediated renal fibrosis.
  • Targeting the TNC-macrophage-TLR4 axis presents a promising therapeutic strategy for kidney fibrosis.