ReviewBiology direct2025
The role of TRIM proteins in the pathogenesis of mycobacterium tuberculosis.
Review in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- TRIM62 promotes osteoarthritis progression by facilitating GPX4 ubiquitination and chondrocyte ferroptosis.American journal of translational research · 2026Article
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis (Mtb) is an intracellular pathogen responsible for tuberculosis (TB), a disease that remains the leading infectious cause of death worldwide. Several host cell proteins have been reported to play a significant role in regulating Mtb infection and replication. Among these, TRIM proteins are a large family of E3 ubiquitin ligases that have been described as being involved in host defence against Mtb, by controlling two important cellular processes: autophagy and the inflammatory response. Autophagy is a highly conserved cellular process deputed to the degradation of damaged or unnecessary components, such as organelles and protein aggregates. Autophagy is induced by a variety of stress stimuli, including nutrient deprivation, hypoxia, infection, oxidative stress and DNA damage, to maintain cellular homeostasis and survival. Autophagy plays a crucial role in host defense against infections by selectively targeting and delivering intracellular pathogens, like bacteria, viruses, and parasites to the lysosomes for degradation. Inflammation is a biological coordinated cellular process involving the secretion of cytokines and chemokines by innate immune cells, that can be triggered by various factors, including damaged cells, toxins and pathogens. Pathogen-Associated Molecular Patterns (PAMPs), found on microbes, are recognized by pattern recognition receptors (PRRs) on immune cells, which trigger signaling pathways leading to pro-inflammatory responses and the elimination of the pathogen. Danger-Associated Molecular Patterns (DAMPs) are host-derived molecules released from damaged cells that activate the same PRRs to initiate or perpetuate inflammation. In this review, we discuss the emerging role played by TRIM proteins in regulating autophagy and pro-inflammatory response during Mtb infection, pointing out the crucial role of TRIM in the complex crosstalk between these processes.Clinical trial number Not applicable.
Indexed as
Identifiers
What Socratic 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 Socratic graph.