Related Experiment Video

Updated: May 4, 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

1.8K

Autophagy activation reduces renal tubular injury induced by urinary proteins

Wei Jing Liu1, Mian-Na Luo1, Jin Tan1

  • 1Institute of Nephrology; Guangdong Medical College; Zhanjiang, China.

Autophagy
|December 19, 2013
PubMed

Insights

Autophagy protects kidney tubular cells from urinary protein damage. Enhancing autophagy reduces injury markers and cell death, while blocking it worsens damage, indicating its protective role.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Autophagy is known to protect against drug-induced kidney injury.
  • The role of autophagy in renal tubular epithelial cells (TECs) during urinary protein overload is not fully understood.

Purpose of the Study:

  • To investigate the role and activity of autophagy in TECs under conditions of urinary protein overload.
  • To determine if autophagy can protect TECs from injury induced by urinary proteins.

Main Methods:

  • Studied autophagy activity in TECs from minimal change nephrotic syndrome (MCNS) patients and a rat model of proteinuria.
  • Utilized HK-2 cells exposed to urinary proteins, analyzing autophagosome/autolysosome formation, SQSTM1/p62 levels, LC3-II turnover, and lysosomal clustering.
  • Investigated the involvement of reactive oxygen species (ROS) and tested the effects of rapamycin (autophagy enhancer) and chloroquine/BECN1 siRNAs (autophagy inhibitors).

Main Results:

  • Increased autophagic vacuoles were observed in TECs from MCNS patients and proteinuric rats.
  • Urinary proteins in HK-2 cells increased autophagosome/autolysosome formation, decreased SQSTM1/p62, and promoted lysosomal turnover via a ROS-dependent pathway.
  • Rapamycin treatment reduced injury markers (LCN2/NGAL, HAVCR1/KIM-1) and apoptosis, while autophagy inhibition worsened these outcomes.
  • In vivo studies corroborated these findings with rapamycin and chloroquine treatments.

Conclusions:

  • Urinary protein overload triggers an increase in autophagic flux in TECs.
  • This enhanced autophagy represents an adaptive response that offers protection against urinary protein-induced kidney injury.
  • Targeting autophagy may be a therapeutic strategy for managing kidney diseases associated with proteinuria.
Keywords:
apoptosisautophagic activationautophagic pathwaytubular epithelial cellsurinary proteins

More Related Videos

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

700
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

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 Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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...
2.3K
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
559
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...
527
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
5.0K
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
99
Drug Elimination by Renal Route: Tubular Reabsorption01:22

Drug Elimination by Renal Route: Tubular Reabsorption

During the process of renal excretion, as the glomerular filtrate progresses to the distal convoluted tubule (DCT), drugs that are highly permeable, lipophilic, and nonionized undergo passive reabsorption from the tubular fluid into the surrounding peritubular capillaries. This reabsorption process restricts their elimination through the kidneys. However, the majority of drugs are either weak acids or weak bases, and their ionization level is dependent on pH. By altering the pH of urine, the...
4.6K