ReviewInternational journal of biological sciences2026
Reprogrammed Fibrotic Niche Fuels Lung Cancer Initiation and Reciprocal Remodeling.
Review in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Exercise interventions remodel the aging microenvironment to improve prognosis in older patients with cancer.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary Fibrosis (PF), an end-stage manifestation of interstitial lung diseases, is associated with largely unfavorable prognoses. Lung cancer (LC), a leading cause of nationally cancer-related mortality with progressively increasing incidence, exhibits pathological interconnections with PF. The chronic remodeling of the pulmonary microenvironment-including cellular components, extracellular matrix (ECM), inflammatory cytokine networks, and metabolic reprogramming-represents the core pathogenic mechanism underlying PF-LC comorbidity. This review systematically elaborates how the fibrotic microenvironment promotes malignant transformation of lung cancer via chronic inflammation, increased matrix stiffness, immunosuppressive regulation, and epigenetic modulation. Furthermore, we investigate the bidirectional crosstalk by which LC progression reciprocally modulates fibrotic processes. Finally, we integrate current clinical challenges and propose novel therapeutic strategies targeting the fibrotic microenvironment to address this lethal pathophysiological synergy.
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Registered trials
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