ArticleThe Journal of biological chemistry2020
Mycobacterium tuberculosis infection up-regulates MFN2 expression to promote NLRP3 inflammasome formation.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- EspF acts as a molecular scaffold to facilitate TRIM25-mediated NLRP3 inflammasome activation during mycobacterial infection.Virulence · 2026Article
- Structural and Functional Alterations of MAMs and Their Immunomodulatory Roles in Sepsis-Induced Lung Injury.Journal of immunology research · 2026Review
- Mitochondria-associated membranes in heart failure: from molecular mechanisms to therapeutic targets.Frontiers in physiology · 2026Review
- Bidirectional Regulation of NLRP3 Inflammasome and Mitochondrial Quality Control in Sepsis: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- Mycobacterium tuberculosis manipulates LINC02528 in macrophages to modulate anti-tuberculosis metabolic immunity.PLoS pathogens · 2025Article
- Calcium signalling and organelle crosstalk in cardiovascular disease: an interplay of cardiac cell death pathways.Molecular biology reports · 2025Review
- Export of eDNA is a mechanism used by Mycobacterium avium subsp. hominissuis for survival within host macrophages.Archives of microbiology · 2025Article
- Mitochondrial dynamics in diabetic peripheral neuropathy: Pathogenesis, progression, and therapeutic approaches.Medicine · 2025Review
- Plasma NLRC4 and NLRP3 as potential diagnostic biomarkers for non-small cell lung cancer in pulmonary tuberculosis.Discover oncology · 2025Article
- Advances in Bacterial Lysate Immunotherapy for Infectious Diseases and Cancer.Journal of immunology research · 2024Review
- Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy.Immunity, inflammation and disease · 2023Review
- Large yellow croaker (Marine life science & technology · 2023Article
- Role of UPRFrontiers in cellular and infection microbiology · 2023Review
- Review
- Activation and Pharmacological Regulation of Inflammasomes.Biomolecules · 2022Review
- The Role of NLRP3 Inflammasome in Alzheimer's Disease and Potential Therapeutic Targets.Frontiers in pharmacology · 2022Review
- Interaction of Mycobacteria With Host Cell Inflammasomes.Frontiers in immunology · 2022Review
- The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Review
- Mitochondrial Fusion Mediated by Mitofusin 1 Regulates Macrophage Mycobactericidal Activity by Enhancing Autophagy.Infection and immunity · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis (TB), caused by the infection of Mycobacterium tuberculosis (MTB), is one of the leading causes of death worldwide, especially in children. However, the mechanisms by which MTB infects its cellular host, activates an immune response, and triggers inflammation remain unknown. Mitochondria play important roles in the initiation and activation of the nucleotide-binding oligomerization domain-like receptor with a pyrin domain 3 (NLRP3) inflammasome, where mitochondria-associated endoplasmic reticulum membranes (MAMs) may serve as the platform for inflammasome assembly and activation. Additionally, mitofusin 2 (MFN2) is implicated in the formation of MAMs, but, the roles of mitochondria and MFN2 in MTB infection have not been elucidated. Using mircroarry profiling of TB patients and in vitro MTB stimulation of macrophages, we observed an up-regulation of MFN2 in the peripheral blood mononuclear cells of active TB patients. Furthermore, we found that MTB stimulation by MTB-specific antigen ESAT-6 or lysate of MTB promoted MFN2 interaction with NLRP3 inflammasomes, resulting in the assembly and activation of the inflammasome and, subsequently, IL-1β secretion. These findings suggest that MFN2 and mitochondria play important role in the pathogen-host interaction during MTB infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.