ArticlePloS one2016
Cleavage of Type I Collagen by Fibroblast Activation Protein-α Enhances Class A Scavenger Receptor Mediated Macrophage Adhesion.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Mechanosignaling promotes macrophage apoptosis resistance in pulmonary fibrosisbioRxiv : the preprint server for biology · 2026Article
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- Collagen dynamics in the breast cancer tumor microenvironment and therapeutic perspectives.Discover oncology · 2025Review
- Profibrotic immune cells and fibro-adipogenic progenitors contribute to skeletal muscle extracellular matrix remodeling and fibrosis in cancer cachexia.American journal of physiology. Cell physiology · 2025Article
- Macrophages and fibroblasts as regulators of the immune response in pancreatic cancer.Nature immunology · 2025Review
- Cancer associated fibroblasts in cancer development and therapy.Journal of hematology & oncology · 2025Review
- PDGF-BB/EGR1 Axis Drives Fibroblast Activation Protein Expression to Promote Abdominal Aortic Aneurysm.International journal of medical sciences · 2025Article
- Cancer-associated fibroblasts: heterogeneity, tumorigenicity and therapeutic targets.Molecular biomedicine · 2024Review
- Fibrillar extracellular matrix produced by pericyte-like cells facilitates glioma cell dissemination.Brain pathology (Zurich, Switzerland) · 2024Article
- CAF-induced physical constraints controlling T cell state and localization in solid tumours.Nature reviews. Cancer · 2024Review
- Tissue Mechanics and Hedgehog Signaling Crosstalk as a Key Epithelial-Stromal Interplay in Cancer Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Modulation of the tumor microenvironment and mechanism of immunotherapy-based drug resistance in breast cancer.Molecular cancer · 2024Review
- From basic research to clinical application: targeting fibroblast activation protein for cancer diagnosis and treatment.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma or a Metaphor for Heterogeneity: From Single-Cell Analysis to Whole-Body Imaging.Biomedicines · 2024Review
- Targeting FAPActa pharmaceutica Sinica. B · 2024Article
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
- Fibroblast diversity and plasticity in the tumor microenvironment: roles in immunity and relevant therapies.Cell communication and signaling : CCS · 2023Review
- [European journal of nuclear medicine and molecular imaging · 2023Article
- Article
- A Quick Guide to CAF Subtypes in Pancreatic Cancer.Cancers · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pathophysiological conditions such as fibrosis, inflammation, and tumor progression are associated with modification of the extracellular matrix (ECM). These modifications create ligands that differentially interact with cells to promote responses that drive pathological processes. Within the tumor stroma, fibroblasts are activated and increase the expression of type I collagen. In addition, activated fibroblasts specifically express fibroblast activation protein-α (FAP), a post-prolyl peptidase. Although FAP reportedly cleaves type I collagen and contributes to tumor progression, the specific pathophysiologic role of FAP is not clear. In this study, the possibility that FAP-mediated cleavage of type I collagen modulates macrophage interaction with collagen was examined using macrophage adhesion assays. Our results demonstrate that FAP selectively cleaves type I collagen resulting in increased macrophage adhesion. Increased macrophage adhesion to FAP-cleaved collagen was not affected by inhibiting integrin-mediated interactions, but was abolished in macrophages lacking the class A scavenger receptor (SR-A/CD204). Further, SR-A expressing macrophages localize with activated fibroblasts in breast tumors of MMTV-PyMT mice. Together, these results demonstrate that FAP-cleaved collagen is a substrate for SR-A-dependent macrophage adhesion, and suggest that by modifying the ECM, FAP plays a novel role in mediating communication between activated fibroblasts and macrophages.
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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.