ReviewExperimental & molecular medicine2019
Autophagy-activating strategies to promote innate defense against mycobacteria.
Review in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 68 citations in OpenAlex.
- Protective mechanism of action of the antifungal drug naftifine againstAntimicrobial agents and chemotherapy · 2026Article
- Autophagy andFrontiers in cellular and infection microbiology · 2026Review
- Autophagy in tuberculosis: advances, translational gaps, and the promise of host-directed therapies.Frontiers in cellular and infection microbiology · 2026Review
- Targeting Autophagy as a Strategy for Developing New Host-Directed Therapeutics Against Nontuberculous Mycobacteria.Pathogens (Basel, Switzerland) · 2025Review
- Immune-endocrine crossroads: the impact of nuclear receptors in Tuberculosis and Chagas disease.Frontiers in endocrinology · 2025Review
- Lessons from cross-pathogen studies: understanding the metabolic rewiring of macrophages upon infection.Frontiers in cellular and infection microbiology · 2025Review
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
- An integrative and comprehensive analysis of blood transcriptomes combined with machine learning models reveals key signatures for tuberculosis diagnosis and risk stratification.Frontiers in microbiology · 2025Article
- Development of a four autophagy-related gene signature for active tuberculosis diagnosis.Frontiers in cellular and infection microbiology · 2025Article
- Review
- Review
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- Article
- Using Zebrafish to Dissect the Interaction of Mycobacteria with the Autophagic Machinery in Macrophages.Biology · 2023Article
- BORC complex specific components and Kinesin-1 mediate autophagy evasion by the autophagy-resistant Mycobacterium tuberculosis Beijing strain.Scientific reports · 2023Article
- Bi-Directional Relationship Between Autophagy and Inflammasomes in Neurodegenerative Disorders.Cellular and molecular neurobiology · 2023Review
- Chemical modulation of SQSTM1/p62-mediated xenophagy that targets a broad range of pathogenic bacteria.Autophagy · 2022Article
- Host-Directed Therapies for Tuberculosis.Pathogens (Basel, Switzerland) · 2022Review
- Host Cell Antimicrobial Responses againstInternational journal of molecular sciences · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.