ReviewJournal of translational medicine2025
Recent advances in TAM mechanisms in lung diseases.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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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.
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Who cites it
6 citing papers in PubMed.
- Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution.bioRxiv : the preprint server for biology · 2026Article
- MerTK Inhibition Aggravates Pancreatic Inflammation and Structural Damage via the NF-κB Pathway in an in vivo Type 2 Diabetic Rat Model.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Efferocytosis in myocardial infarction: the regulatory core from inflammation resolution to cardiac repair.Frontiers in immunology · 2026Review
- Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition.Frontiers in immunology · 2026Review
- Comprehensive Genomic Profiling of Small-Cell Lung Cancer Reveals Frequent Potentially Targetable Alterations.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TYRO3, MERTK, and AXL receptor tyrosine kinases, collectively known as TAM receptors, play a vital role in maintaining lung tissue homeostasis by regulating integrity and self-renewal. These receptors activate signalling pathways that inhibit apoptosis, promote cell proliferation and differentiation, mediate cell adhesion and migration, and perform other essential biological functions. Additionally, TAM receptors are implicated in mechanisms that suppress anti-tumor immunity and confer resistance to immune checkpoint inhibitors. Disruption of the homeostatic balances can lead to pathological conditions such as lung inflammation, fibrosis, or tumors. Recent studies highlight their significant role in COVID-19-induced lung injury. However, the exact mechanisms by which TAM receptors contribute to lung diseases remain unclear. This article reviews the potential mechanisms of TAM receptor involvement in disease progression, focusing on lung inflammation, fibrosis, cancer, and COVID-19-induced lung injury. It also explores future research aspects and the therapeutic potentials of targeting TAM receptors, providing a theoretical foundation for understanding lung disease mechanisms and identifying treatment targets.
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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.