ArticleThe Journal of infectious diseases2025
Troglitazone Reduction of Intracellular Mycobacterium tuberculosis Survival Via Macrophage Autophagy Through LKB1-AMPKα Signaling.
Article in The Journal of infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Association Between Thiazolidinedione Therapy and Tuberculosis-Related Events in Type 2 Diabetes: A Population-Based Cohort Study.Microorganisms · 2026Article
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- EliminateJournal of medical microbiology · 2026Article
- Autophagy in tuberculosis: advances, translational gaps, and the promise of host-directed therapies.Frontiers in cellular and infection microbiology · 2026Review
- Lipid metabolism in the resuscitation of dormant mycobacterium tuberculosis: molecular resilience, host hijacking, and clinical opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Autophagy andFrontiers in cellular and infection microbiology · 2026Review
- Nanomedicine strategies for cuproptosis: Metabolic reprogramming and tumor immunotherapy.Acta pharmaceutica Sinica. B · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Tuberculosis caused by Mycobacterium tuberculosis (Mtb), results in significant disease and death worldwide. Host-directed therapy, including conventional drugs, is a promising antituberculosis strategy that shows synergistic antibacterial effects when combined with antituberculosis drugs. Here, the mycobactericidal effect of 3 antidiabetic drugs was examined. Of these, only troglitazone (Trog) enhanced the antimycobacterial effect in vitro and in vivo. This was due to Trog-mediated autophagy activation. Moreover, a knock-down experiment revealed that Trog activated autophagy and exhibited antimycobacterial activity through the serine/threonine-protein kinase STK11 (LKB1)-5'-AMP-activated protein kinase (AMPK) signaling pathway. Molecular docking and coimmunoprecipitation experiments demonstrated that Trog promoted LKB1 phosphorylation and activation by targeting STE20-related kinase adapter protein alpha (STRADA). Finally, we found that Trog inhibited the intracellular survival of clinical isoniazid-resistant Mtb, and the combination of Trog and isoniazid showed additive antibacterial effects against Mtb H37Rv. Taken together, antidiabetic Trog may be repurposed as a candidate for host-directed therapy and combined with first-line antituberculosis drugs.
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Registered trials
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