Related Experiment Video

Updated: Mar 28, 2026

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

Metformin Inhibits Inflammation by Targeting the NLRP3 Inflammasome: Linking NF-κB/NEK7/AMPK Signaling to

Dingyi Ning1,2, Chenxin Jiang1, Jiangyan Zeng3

  • 1Queen Mary School, Nanchang University, Nanchang, 330006, People's Republic of China.

Journal of Inflammation Research
|March 27, 2026
PubMed

Insights

Metformin, a diabetes drug, reduces inflammation by impacting mitochondria and inhibiting NLRP3 inflammasome activation. This suggests potential for treating various diseases beyond diabetes.

Area of Science:

  • * Pharmacology
  • * Immunology
  • * Cellular Biology

Background:

  • * Metformin is a primary treatment for type 2 diabetes.
  • * It possesses anti-inflammatory properties beyond glucose control.
  • * Its role in inhibiting the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is established, but mitochondrial involvement requires further study.

Purpose of the Study:

  • * To review how metformin regulates inflammation via multiple pathways.
  • * To elucidate the role of mitochondria in metformin's anti-inflammatory effects.
  • * To explore metformin's potential in treating inflammasome-driven diseases.

Main Methods:

  • * Literature review of studies on metformin, inflammation, and mitochondria.
  • * Analysis of metformin's effects on key inflammasome pathways (TLR4/NF-κB, NEK7, AMPK, JAK2-STAT).
  • * Examination of metformin's impact on mitochondrial functions related to NLRP3 activation.

Main Results:

  • * Metformin regulates inflammation through TLR4/NF-κB, NEK7, AMPK, and JAK2-STAT pathways, involving mitochondria.
  • * Metformin's mitochondrial effects inhibit NLRP3 activation steps: NEK7 assembly, reactive oxygen species (ROS) production, thioredoxin-interacting protein (TXNIP) expression, and caspase 1 activity.
  • * Metformin reduces IL-1β/IL-18 maturation.

Conclusions:

  • * Metformin modulates NLRP3 inflammasome activation through mitochondrial regulation.
  • * Metformin shows promise for treating multi-organ diseases associated with inflammasome pathways.
  • * Clinical trials are warranted to assess metformin's efficacy in NLRP3 inflammasome-driven pathologies beyond diabetes.
Keywords:
elucidation of mechanisminflammasomemetforminmulti-organ diseasessignaling pathways

More Related Videos

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.8K
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

7.9K

Related Concept Videos

Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
922
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
10.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.3K
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
1.0K
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
6.0K
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
663