ReviewBiologia futura2026
PI3K/PKB signaling network as a host target to enhance bacterial ingestion and clearance.
Review in Biologia futura, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibiotic resistance, driven by the misuse of antibiotics and the slow pace of new drug development, has led to a global rise in multidrug-resistant bacteria (MDRB), posing a major public health challenge. Host-directed therapies that enhance innate immune responses offer promising alternatives to traditional antibiotics. This review focuses on the central role of the PI3K/PKB (Akt) signaling pathway in phagocytosis and bacterial inactivation across both primitive phagocytes, such as Dictyostelium discoideum, and mammalian immune cells. In Dictyostelium, PI3K/PKB signaling coordinates the maturation of phagosomes and the fusion of phagolysosomes, processes essential for bacterial killing. Similarly, in immune cells, this pathway regulates cytoskeletal remodeling, vesicle trafficking, and the degradation of microbes. Specific pathogens, including Mycobacterium tuberculosis and Salmonella, subvert PI3K/PKB to evade immune responses, highlighting the pathway's dual role in host defense and pathogen survival. Targeting PI3K/PKB signaling or its inhibitory regulators may enhance phagocytic efficiency and restore immune function. Thus, PI3K/PKB represents a critical module in innate immunity and a compelling target for next-generation antimicrobial strategies.
Indexed as
Identifiers
41296200What 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.