Overexpression of sirtuin 1 attenuates calcium oxalate-induced kidney injury by promoting macrophage polarization

Related Experiment Video

Updated: Jul 30, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
10:07

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

66.6K

Bao-Feng Song1, Bo-Jun Li1, Jin-Zhuo Ning1

  • 1Department of Urology, Renmin Hospital of Wuhan University, Wuhan, China.

International Immunopharmacology
|June 10, 2023
PubMed

Insights

Sirtuin 1 (SIRT1) protein helps macrophages fight kidney stones by promoting anti-inflammatory responses. This reduces kidney cell injury and crystal deposition, suggesting SIRT1 as a potential therapeutic target for kidney stones.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Kidney stones involve inflammation and macrophage infiltration.
  • The roles of Sirtuin 1 (SIRT1) and NOTCH signaling in kidney stone-related injury are unclear.
  • Understanding SIRT1's mechanism in calcium oxalate (CaOx) deposition is crucial.

Purpose of the Study:

  • To investigate SIRT1's role in macrophage polarization during CaOx deposition.
  • To explore the relationship between SIRT1 and NOTCH signaling in kidney injury.
  • To determine if SIRT1 can inhibit CaOx crystal deposition and renal cell damage.

Main Methods:

  • Analysis of public single-cell sequencing data.
  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR).
  • Immunostaining and Western blotting techniques.

Main Results:

  • SIRT1 expression decreased in macrophages exposed to CaOx or kidney stones.
  • Overexpression of SIRT1 promoted anti-inflammatory M2 macrophage polarization, reducing kidney injury in hyperoxuria models.
  • Reduced SIRT1 activated NOTCH signaling, leading to pro-inflammatory M1 polarization.

Conclusions:

  • SIRT1 promotes M2 macrophage polarization by inhibiting NOTCH signaling.
  • This mechanism reduces CaOx deposition, apoptosis, and kidney damage.
  • SIRT1 is a potential therapeutic target for kidney stone disease progression.
Keywords:
CaOxKidney stoneMacrophageNotchPolarizationSIRT1

More Related Videos

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis07:45

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Published on: November 28, 2015

35.6K
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry07:14

Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry

Published on: October 18, 2016

14.9K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...