GO:2000271 positive regulation of fibroblast apoptotic process: Apoptosis Signaling Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:2000271 describes any process that activates or increases the frequency, rate or extent of fibroblast apoptotic process, a tightly regulated form of programmed cell death in fibroblasts.
• Key molecular players include BAX, caspase-3, RIPK1, MERTK, WT1, FUT8, CD36, NAMPT, and COL8A1, which modulate fibroblast survival or death in fibrotic and malignant contexts.
• Dysregulation of fibroblast apoptosis contributes to pulmonary fibrosis, kidney fibrosis, cancer-associated fibroblast persistence, and pterygium pathogenesis.
• Experimental models for studying this process include knockout, point-mutation, knock-in, and overexpression cell lines, as well as CRISPR library screening and bioinformatics analysis.
• The process is regulated by mitochondrial-dependent apoptosis pathways, death receptor signaling, and crosstalk with autophagy and necroptosis machinery.
• Targeting positive regulators of fibroblast apoptosis is a promising therapeutic strategy for fibrotic diseases and cancers driven by fibroblast accumulation.
Description
Fibroblasts are the principal effector cells of connective tissue homeostasis, and their aberrant survival or death underlies a wide range of pathological conditions, including organ fibrosis and tumor progression. The Gene Ontology term GO:2000271, positive regulation of fibroblast apoptotic process, captures the biological processes that actively promote the programmed death of fibroblasts. This term is essential for researchers dissecting the molecular switches that determine whether fibroblasts persist or are eliminated in response to injury, inflammation, or oncogenic stress. Understanding positive regulation of fibroblast apoptosis has direct translational implications: excessive fibroblast apoptosis can impair tissue repair, whereas insufficient apoptosis drives fibrotic remodeling and cancer-associated fibroblast accumulation. Recent studies have identified specific regulators, such as RUBCNL/PACER, which represses RIPK1-dependent apoptosis and necroptosis, and MERTK, whose suppression promotes apoptosis in pterygium fibroblasts. These findings highlight the therapeutic potential of modulating fibroblast apoptosis in diseases such as idiopathic pulmonary fibrosis, acute kidney injury-chronic kidney disease transition, and colorectal cancer.
positive regulation of fibroblast apoptotic process At A Glance
| GO ID | GO:2000271 |
|---|---|
| GO term | positive regulation of fibroblast apoptotic process |
| Ontology | biological_process |
| Synonym | positive regulation of fibroblast apoptosis |
| Definition | Any process that activates or increases the frequency, rate or extent of fibroblast apoptotic process. |
| Major function | Promotion of programmed cell death in fibroblasts, influencing tissue remodeling, fibrosis, and tumor microenvironment. |
| Related processes | Apoptotic signaling, mitochondrial-dependent apoptosis, death receptor pathways, autophagy crosstalk. |
| Key regulators | BAX, caspase-3, RIPK1, MERTK, WT1, FUT8, CD36, NAMPT, COL8A1. |
| Disease relevance | Pulmonary fibrosis, kidney fibrosis, cancer-associated fibroblasts, pterygium. |
What Is GO:2000271?
GO:2000271, positive regulation of fibroblast apoptotic process, is defined as any process that activates or increases the frequency, rate or extent of fibroblast apoptotic process. In other words, it encompasses all molecular events and signaling pathways that promote the execution of programmed cell death specifically in fibroblasts, as opposed to merely being associated with apoptosis in general.
Why Is positive regulation of fibroblast apoptotic process Important in Cell Biology?
Positive regulation of fibroblast apoptotic process is critical because fibroblasts are central to wound healing, tissue remodeling, and the pathogenesis of fibrosis and cancer. The balance between fibroblast survival and apoptosis determines whether normal tissue architecture is restored or pathological accumulation occurs. For example, in idiopathic pulmonary fibrosis, impaired apoptotic clearance of fibroblasts leads to persistent fibrotic lesions, and Wilms tumor 1 (WT1) has been shown to impair apoptotic clearance of fibroblasts in distal fibrotic lung lesions. In acute kidney injury transitioning to chronic kidney disease, FUT8-mediated core fucosylation of CD36 accelerates pericyte-myofibroblast transition through mitochondrial-dependent apoptosis, highlighting how specific glycosylation events can drive fibroblast fate. In colorectal cancer, COL8A1-positive cancer-associated fibroblasts promote 5-fluorouracil resistance, suggesting that targeting their survival or inducing their apoptosis could improve chemotherapy response. Therefore, understanding the positive regulation of fibroblast apoptosis offers mechanistic insights and therapeutic opportunities across fibrotic and malignant diseases.
• Controls tissue homeostasis by eliminating excess or damaged fibroblasts after injury.
• Dysregulation leads to fibrotic diseases such as pulmonary fibrosis and kidney fibrosis.
• Modulates tumor microenvironment by affecting cancer-associated fibroblast persistence.
• Involves mitochondrial-dependent apoptosis pathways regulated by BAX and caspase-3.
• Crosstalks with autophagy and necroptosis via RIPK1 and RUBCNL/PACER.
• MERTK suppression promotes apoptosis in pterygium fibroblasts, offering a therapeutic target.
• WT1 impairs apoptotic clearance of fibroblasts in fibrotic lung lesions.
• NAMPT orchestrates fibroblast cuproptosis and immune crosstalk in IPF progression.
• FUT8-mediated CD36 core fucosylation accelerates pericyte-myofibroblast transition via apoptosis.
• COL8A1-positive CAFs drive 5-FU resistance, linking fibroblast apoptosis to chemoresistance.
What Happens During positive regulation of fibroblast apoptotic process?
Initiation of Apoptotic Signaling in Fibroblasts
In simple terms: The process starts when a fibroblast receives a death signal, either from outside the cell or from internal stress.
Positive regulation of fibroblast apoptosis begins with the activation of pro-apoptotic signaling pathways. External stimuli such as death ligands or internal stressors like DNA damage can trigger this process. Key initiators include the mitochondrial-dependent pathway, where BAX activation leads to mitochondrial outer membrane permeabilization, and death receptor pathways that activate caspase-8. In pulmonary fibroblasts, propyl gallate induces cell death through regulation of Bax and caspase-3, demonstrating that these core apoptotic machinery components are directly involved in positive regulation. Additionally, RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis, indicating that relief of this repression can promote fibroblast apoptosis.
Mitochondrial Outer Membrane Permeabilization and Cytochrome c Release
In simple terms: The mitochondria become leaky, releasing factors that activate the cell death executioners.
Upon apoptotic stimulation, BAX and BAK undergo conformational changes and oligomerize on the mitochondrial outer membrane, leading to membrane permeabilization. This releases cytochrome c into the cytosol, which binds APAF-1 to form the apoptosome, activating caspase-9. This mitochondrial-dependent apoptosis pathway is critical in fibroblasts; for instance, FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through the mitochondrial-dependent apoptosis pathway during AKI-CKD. This step is a point of regulation by anti-apoptotic BCL-2 family proteins, and its positive regulation ensures commitment to cell death.
Caspase Activation and Execution of Apoptosis
In simple terms: A cascade of enzymes called caspases dismantles the cell in an orderly way.
The initiator caspases (caspase-8, -9) cleave and activate executioner caspases (caspase-3, -6, -7). Caspase-3 is a key executioner; its activation is a hallmark of fibroblast apoptosis. In human pulmonary fibroblasts, propyl gallate induces cell death through the regulation of Bax and caspase-3, confirming that caspase-3 activation is a central event in positive regulation of fibroblast apoptosis. This execution phase leads to DNA fragmentation, cytoskeletal disassembly, and formation of apoptotic bodies, which are then cleared by phagocytes.
Regulation by Receptor Tyrosine Kinases and Efferocytosis
In simple terms: Cell surface receptors and clearance mechanisms can either promote or inhibit the death process.
MERTK, a receptor tyrosine kinase, is involved in efferocytosis and cell survival. Suppression of MERTK inhibits proliferation and migration of pterygium fibroblasts, and promotes apoptosis, indicating that MERTK negatively regulates fibroblast apoptosis. Conversely, WT1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions, suggesting that WT1 modulates the efferocytosis of apoptotic fibroblasts, thereby affecting the overall rate of apoptosis. These findings highlight that positive regulation of fibroblast apoptosis can occur at the level of death receptor signaling, mitochondrial amplification, and clearance of apoptotic cells.
Crosstalk with Autophagy and Necroptosis
In simple terms: The cell death process is connected to other stress responses like autophagy and necroptosis.
The autophagy protein RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis, meaning that its downregulation or inactivation can enhance fibroblast apoptosis. This crosstalk ensures that fibroblasts integrate multiple stress signals to decide their fate. NAMPT orchestrates fibroblast cuproptosis and immune crosstalk during IPF progression, further illustrating that fibroblast death modalities are interconnected and can be positively regulated by metabolic and immune signals.
Key Genes Involved in GO:2000271 positive regulation of fibroblast apoptotic process
The following genes and proteins have been experimentally implicated in the positive regulation of fibroblast apoptotic process, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| BAX | Pro-apoptotic BCL-2 family member; mediates mitochondrial outer membrane permeabilization | Induced by propyl gallate in pulmonary fibroblasts; marker of mitochondrial apoptosis |
| CASP3 | Executioner caspase; cleaves key cellular substrates during apoptosis | Activated in propyl gallate-induced fibroblast death; central to apoptosis execution |
| RIPK1 | Kinase regulating apoptosis and necroptosis; repressed by RUBCNL/PACER | Its derepression promotes fibroblast apoptosis; crosstalk with autophagy |
| RUBCNL/PACER | Autophagy protein; represses RIPK1-dependent apoptosis and necroptosis | Loss of function enhances fibroblast apoptosis; links autophagy to apoptosis |
| MERTK | Receptor tyrosine kinase; involved in efferocytosis and survival signaling | Suppression promotes apoptosis in pterygium fibroblasts; therapeutic target |
| WT1 | Transcription factor; impairs apoptotic clearance of fibroblasts | Dysregulation in fibrotic lung lesions; affects fibroblast apoptosis clearance |
| FUT8 | Fucosyltransferase; core fucosylation of CD36 | Upregulates CD36 to accelerate pericyte-myofibroblast transition via mitochondrial apoptosis |
| CD36 | Scavenger receptor; mediates lipid uptake and signaling | Core fucosylation by FUT8 promotes mitochondrial-dependent apoptosis in AKI-CKD |
| NAMPT | Nicotinamide phosphoribosyltransferase; regulates NAD+ metabolism | Orchestrates fibroblast cuproptosis and immune crosstalk in IPF |
| COL8A1 | Collagen type VIII alpha 1; component of extracellular matrix | Expressed by cancer-associated fibroblasts; drives 5-FU resistance in colorectal cancer |
| SMAD2/3 | TGF-beta signaling effectors; regulate fibroblast differentiation and survival | Synergize with Wnt to regulate osteogenic differentiation of fibroblasts in ankylosing spondylitis |
| WNT | Secreted signaling proteins; regulate cell fate and proliferation | Synergize with Smad signaling in fibroblast differentiation; potential crosstalk with apoptosis |
| BCL-2 | Anti-apoptotic protein; inhibits BAX/BAK | Not directly cited in provided references, but implied as counter-regulator of BAX |
| APAF-1 | Apoptosome component; activates caspase-9 | Not directly cited in provided references, but part of mitochondrial apoptosis pathway |
| CASP9 | Initiator caspase; activated by apoptosome | Not directly cited in provided references, but downstream of mitochondrial permeabilization |
| CASP8 | Initiator caspase; activated by death receptors | Not directly cited in provided references, but part of extrinsic apoptosis pathway |
| FADD | Adaptor protein; mediates death receptor signaling | Not directly cited in provided references, but involved in extrinsic apoptosis |
| TNFRSF10A/B | Death receptors for TRAIL; activate extrinsic apoptosis | Not directly cited in provided references, but potential regulators of fibroblast apoptosis |
How Is positive regulation of fibroblast apoptotic process Regulated?
The positive regulation of fibroblast apoptotic process is controlled at multiple levels. At the transcriptional level, WT1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions, suggesting that WT1 modulates the expression of genes involved in efferocytosis and apoptosis. Post-translational modifications, such as core fucosylation of CD36 by FUT8, can direct fibroblasts toward mitochondrial-dependent apoptosis during AKI-CKD. Receptor tyrosine kinase signaling through MERTK suppresses apoptosis in pterygium fibroblasts, and its inhibition promotes cell death. Furthermore, the autophagy protein RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis, indicating that autophagy machinery can negatively regulate fibroblast apoptosis. Metabolic regulators like NAMPT orchestrate fibroblast cuproptosis and immune crosstalk in IPF, linking NAD+ metabolism to fibroblast death. These diverse regulatory inputs ensure that fibroblast apoptosis is tightly controlled in response to environmental cues.
positive regulation of fibroblast apoptotic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| WT1 | Pulmonary fibrosis; impaired apoptotic clearance | WT1 knockout or overexpression in human lung fibroblasts; bleomycin-induced fibrosis model |
| FUT8 | AKI-CKD; pericyte-myofibroblast transition | FUT8 knockout or knockdown in pericytes/fibroblasts; unilateral ureteral obstruction model |
| MERTK | Pterygium; fibroblast proliferation and migration | MERTK knockout or inhibitor treatment in pterygium fibroblasts; cell viability and apoptosis assays |
| COL8A1 | Colorectal cancer; 5-FU resistance | COL8A1 knockout in cancer-associated fibroblasts; co-culture with colorectal cancer cells and 5-FU treatment |
| NAMPT | IPF; cuproptosis and immune crosstalk | NAMPT knockout or overexpression in lung fibroblasts; bleomycin model and immune cell co-culture |
Pulmonary Fibrosis and Impaired Fibroblast Apoptosis
Idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of apoptosis-resistant fibroblasts and myofibroblasts, leading to progressive scarring. WT1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions, contributing to fibrosis persistence. NAMPT orchestrates fibroblast cuproptosis and immune crosstalk during IPF progression, suggesting that metabolic reprogramming influences fibroblast death modalities. Therefore, strategies that positively regulate fibroblast apoptosis may reduce fibrotic burden.
Kidney Fibrosis and Mitochondrial-Dependent Apoptosis
In acute kidney injury transitioning to chronic kidney disease (AKI-CKD), FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through the mitochondrial-dependent apoptosis pathway. This highlights how glycosylation events can promote fibroblast apoptosis and contribute to maladaptive repair. Targeting FUT8 or CD36 may modulate fibroblast apoptosis in kidney fibrosis.
Cancer-Associated Fibroblasts and Chemoresistance
COL8A1-positive cancer-associated fibroblasts are drivers of 5-fluorouracil resistance in colorectal cancer. These fibroblasts likely evade apoptosis, supporting tumor survival. Positive regulation of fibroblast apoptosis could sensitize tumors to chemotherapy by depleting pro-tumorigenic fibroblasts. Thus, understanding the apoptotic pathways in CAFs is clinically relevant.
Pterygium and Ocular Fibroblast Apoptosis
Pterygium is a benign fibrovascular growth of the conjunctiva, in which fibroblasts contribute to pathogenesis. Suppression of MERTK inhibits proliferation and migration of pterygium fibroblasts and promotes apoptosis. This suggests that MERTK inhibitors could be used to induce fibroblast apoptosis in pterygium. The study provides a direct link between a specific kinase and positive regulation of fibroblast apoptosis.
From positive regulation of fibroblast apoptotic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate gene increase fibroblast apoptosis? | CRISPR knockout in primary human fibroblasts or cell lines (e.g., BJ, IMR-90) |
| Does a specific point mutation in BAX affect its pro-apoptotic activity? | CRISPR point mutation knock-in of BAX variants in fibroblasts |
| Does tagging an endogenous apoptosis regulator alter its localization or function? | CRISPR knock-in of fluorescent or epitope tags (e.g., GFP, HA) at the endogenous locus |
| Does overexpression of an anti-apoptotic gene reduce fibroblast apoptosis? | CRISPR activation (CRISPRa) or lentiviral overexpression in fibroblasts |
| Which genes regulate fibroblast apoptosis in a genome-wide manner? | CRISPR library screening (GeCKO, Brunello) in fibroblasts under apoptotic stimuli |
| Can we identify pathways enriched in fibroblast apoptosis? | Bioinformatics analysis of RNA-seq or proteomics data from knockout/overexpression models |
How to Study the positive regulation of fibroblast apoptotic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Annexin V/PI flow cytometry | Phosphatidylserine externalization and membrane integrity | Quantify apoptosis in fibroblasts after gene knockout or drug treatment |
| Caspase-3/7 activity assay | Executioner caspase enzymatic activity | Confirm apoptotic commitment in fibroblasts |
| Western blot | Cleaved caspase-3, PARP, BAX/BCL-2 ratio | Detect mitochondrial apoptosis pathway activation |
| TUNEL assay | DNA fragmentation | Visualize apoptotic nuclei in tissue sections or cultured fibroblasts |
| CRISPR knockout screening | Gene essentiality for apoptosis resistance/sensitivity | Identify positive regulators of fibroblast apoptosis |
| RNA-seq | Transcriptional changes upon apoptotic stimulation | Discover pathways and gene signatures |
| Proteomics | Protein expression and post-translational modifications | Uncover signaling networks in fibroblast apoptosis |
| Immunofluorescence | Localization of apoptosis regulators (e.g., BAX, cytochrome c) | Assess mitochondrial permeabilization in situ |
Flow Cytometry and Annexin V Staining
Flow cytometry with Annexin V and propidium iodide is a standard method to quantify apoptosis in fibroblasts. It measures phosphatidylserine externalization, an early apoptotic event. This method is used to assess the effect of gene knockouts or treatments on positive regulation of fibroblast apoptosis.
Caspase Activity Assays
Caspase-3/7 activity assays using fluorogenic substrates or luminescent kits measure executioner caspase activation. They are widely used to confirm that a stimulus or genetic manipulation promotes apoptosis in fibroblasts.
Western Blotting for Apoptosis Markers
Western blotting detects cleavage of caspase-3, PARP, and changes in BAX/BCL-2 ratio. These markers indicate mitochondrial-dependent apoptosis. This method is essential for mechanistic studies of fibroblast apoptosis.
CRISPR Screening and Bioinformatics
Genome-wide CRISPR knockout or activation screens coupled with next-generation sequencing identify genes that positively or negatively regulate fibroblast apoptosis. Bioinformatics analysis of screen data reveals enriched pathways and networks.
How CRISPR Can Be Used to Study GO:2000271 positive regulation of fibroblast apoptotic process
Knockout
CRISPR knockout is used to delete candidate genes and assess their role in positive regulation of fibroblast apoptosis. For example, knocking out MERTK in pterygium fibroblasts would test whether its loss enhances apoptosis. Similarly, knocking out FUT8 or CD36 can determine their requirement for mitochondrial-dependent apoptosis during AKI-CKD. Knockout models are essential for establishing causality.
Point Mutation
CRISPR point mutation knock-in introduces specific amino acid substitutions to dissect domain functions. For instance, mutating phosphorylation sites in BAX or RIPK1 can reveal their regulatory roles in fibroblast apoptosis. This approach is valuable for understanding how post-translational modifications control apoptotic signaling.
Knock-in
CRISPR knock-in of reporter tags (e.g., GFP, luciferase) or epitope tags at endogenous loci allows real-time monitoring of apoptosis regulators in fibroblasts. Tagging RIPK1 or BAX can reveal their dynamics during apoptosis. Knock-in of disease-associated variants can also model genetic susceptibility to fibrosis.
Overexpression
CRISPR activation (CRISPRa) or lentiviral overexpression is used to increase expression of anti-apoptotic or pro-apoptotic genes. Overexpressing WT1 in fibroblasts can test its ability to impair apoptotic clearance. Overexpressing RUBCNL/PACER can test its repression of RIPK1-dependent apoptosis. These models help identify sufficiency.
How EDITGENE Supports positive regulation of fibroblast apoptotic process Research
Researchers studying positive regulation of fibroblast apoptotic process-related genes often need to determine whether a candidate gene is causally involved in promoting or inhibiting fibroblast death. EDITGENE provides comprehensive CRISPR-based services to enable such functional studies with high precision and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of fibroblast apoptotic process research.
Frequently Asked Questions About positive regulation of fibroblast apoptotic process
What is GO:2000271 positive regulation of fibroblast apoptotic process?
GO:2000271 is a Gene Ontology biological process term defined as any process that activates or increases the frequency, rate or extent of fibroblast apoptotic process.
What genes are involved in positive regulation of fibroblast apoptotic process?
Key genes include BAX, CASP3, RIPK1, RUBCNL/PACER, MERTK, WT1, FUT8, CD36, NAMPT, and COL8A1, as shown in recent studies.
How is fibroblast apoptosis regulated?
It is regulated by mitochondrial-dependent pathways, death receptor signaling, autophagy crosstalk, and receptor tyrosine kinases like MERTK.
What diseases are associated with defective fibroblast apoptosis?
Pulmonary fibrosis, kidney fibrosis, pterygium, and colorectal cancer chemoresistance are linked to altered fibroblast apoptosis.
What is the role of BAX in fibroblast apoptosis?
BAX is a pro-apoptotic BCL-2 family member that mediates mitochondrial outer membrane permeabilization, leading to caspase activation and cell death.
How does MERTK affect fibroblast apoptosis?
MERTK suppresses apoptosis; its inhibition promotes apoptosis in pterygium fibroblasts, making it a potential therapeutic target.
What experimental models are used to study positive regulation of fibroblast apoptosis?
CRISPR knockout, point mutation, knock-in, overexpression cell models, and CRISPR library screening are commonly used.
Can CRISPR be used to study fibroblast apoptosis?
Yes, CRISPR knockout, activation, and screening are powerful tools to identify and validate regulators of fibroblast apoptosis.
What is the link between FUT8 and fibroblast apoptosis?
FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through mitochondrial-dependent apoptosis during AKI-CKD.
How does WT1 affect fibroblast apoptosis in lung fibrosis?
WT1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions, contributing to fibrosis persistence.
Conclusion
GO:2000271 positive regulation of fibroblast apoptotic process is a critical biological process that governs fibroblast fate in health and disease. The integration of mitochondrial-dependent apoptosis, death receptor signaling, autophagy crosstalk, and receptor tyrosine kinase regulation determines whether fibroblasts survive or die. Dysregulation of this process contributes to pulmonary fibrosis, kidney fibrosis, pterygium, and cancer chemoresistance. Targeting positive regulators of fibroblast apoptosis holds therapeutic promise, and CRISPR-based models are indispensable for dissecting these mechanisms. EDITGENE offers a comprehensive suite of services to support such research, from knockout and knock-in cell lines to library screening and bioinformatics.
References
- 1. Rojas-Rivera D et al.. 2024. The autophagy protein RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis.. Autophagy 20(11):2444-2459 PMID: 38873940
- 2. Jiang J et al.. 2026. NAMPT orchestrates fibroblast cuproptosis and immune crosstalk during IPF progression.. Front Immunol 17:1726692 PMID: 42245670
- 3. Shang Y et al.. 2024. FUT8 upregulates CD36 and its core fucosylation to accelerate pericyte-myofibroblast transition through the mitochondrial-dependent apoptosis pathway during AKI-CKD.. Mol Med 30(1):222 PMID: 39563263
- 4. Zeng Y et al.. 2022. Wnt and Smad signaling pathways synergistically regulated the osteogenic differentiation of fibroblasts in ankylosing spondylitis.. Tissue Cell 77:101852 PMID: 35753224
- 5. Ediga HH et al.. 2025. Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.. J Clin Invest 135(15) PMID: 40493404
- 6. Park WH. 2024. Propyl gallate induces human pulmonary fibroblast cell death through the regulation of Bax and caspase-3.. Ann Med 56(1):2319853 PMID: 38373208
- 7. Ding M et al.. 2026. COL8A1-positive cancer-associated fibroblasts are drivers of 5-fluorouracil resistance in colorectal cancer.. Apoptosis 31(3) PMID: 41784732
- 8. Ouyang J et al.. 2025. Suppression of MERTK inhibits proliferation and migration of pterygium fibroblasts.. Exp Eye Res 260:110595 PMID: 40849004
