Fibrinogen-like protein 2 regulates inflammatory and metabolic reprogramming of airway smooth muscle cells through PI3K/Akt activation - Report - MDSpire

Fibrinogen-like protein 2 regulates inflammatory and metabolic reprogramming of airway smooth muscle cells through PI3K/Akt activation

  • By

  • Bo Zhao

  • Yanran Che

  • May 12, 2026

  • 0 min

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Clinical Report: Fibrinogen-like Protein 2 Modulates Inflammatory Changes in ASMCs

Overview

This study investigates the role of fibrinogen-like protein 2 (FGL2) in airway smooth muscle cells (ASMCs) and its modulation of inflammatory and metabolic changes via the PI3K/Akt pathway. Silencing FGL2 significantly attenuates PDGF-BB-induced ASMC dysfunction, suggesting its potential as a therapeutic target in chronic airway diseases.

Background

Airway remodeling is a critical feature of chronic airway diseases such as asthma and COPD, characterized by ASMC proliferation and inflammation. Understanding the signaling pathways involved in ASMC dysfunction is essential for developing targeted therapies. FGL2's role in modulating these processes highlights its potential significance in managing airway remodeling.

Data Highlights

ParameterEffect of FGL2 Knockdown
ASMC ProliferationSuppressed
MigrationReduced
Pro-inflammatory CytokinesDecreased (TNF-α, IL-1β, IL-6)
Oxidative StressLowered ROS accumulation
Glycolytic MetabolismInhibited (glucose consumption, lactate production)

Key Findings

  • FGL2 expression is increased in ASMCs upon PDGF-BB stimulation.
  • Silencing FGL2 reduces PI3K/Akt pathway activation, indicated by decreased phosphorylation of PI3K and Akt.
  • FGL2 knockdown leads to decreased ASMC proliferation, migration, and ECM protein expression.
  • Depletion of FGL2 significantly lowers the secretion of pro-inflammatory cytokines.
  • FGL2 knockdown restores antioxidant enzyme activities and reduces oxidative stress.

Clinical Implications

Targeting FGL2 may provide a novel therapeutic approach to mitigate airway remodeling in chronic airway diseases. Understanding its role in ASMC dysfunction could lead to improved management strategies for conditions like asthma and COPD.

Conclusion

FGL2 plays a significant role in modulating inflammatory and metabolic changes in ASMCs through the PI3K/Akt pathway. Further research is warranted to explore its therapeutic potential in chronic airway diseases.

Related Resources & Content

  1. Archives of Toxicology, 2022 -- TRPM7 Modulates Plasmin Activity and Enhances TGF-β1 Signaling in Primary Human Lung Fibroblasts
  2. Basic Research in Cardiology, 2020 -- Inhibition of Plasminogen Activator Inhibitor-1 Mitigates Cardiac Fibrosis and Enhances M2 Macrophage Polarization in Inflammatory Cardiomyopathy
  3. Journal of Crohn's and Colitis -- Therapeutic potential of Janus kinase inhibitors for the management of fibrosis in inflammatory bowel disease
  4. Frontiers in Immunology -- Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming
  5. GINA 2025 Global Strategy for Asthma Management, 2025
  6. GINA 2025 Global Strategy for Asthma Management an
  7. Integrative Roles of Pro‐Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma - PMC
  8. A Multicentre, Randomized, Double-Blind, Placebo-Controlled, Crossover Study To Investigate the Efficacy, Safety, Tolerability, and Pharmacokinetics of Repeat Doses of Inhaled Nemiralisib in Adults with Persistent, Uncontrolled Asthma - PubMed

Original Source(s)

Fibrinogen-like protein 2 regulates inflammatory and metabolic reprogramming of airway smooth muscle cells through PI3K/Akt activation

  • by Bo Zhao, Yanran Che

  • May 12, 2026

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