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Overview of the VEGF Signaling Pathway The VEGF (Vascular Endothelial Growth Factor) signaling pathway is a key regulator of angiogenesis, playing a critical role in both physiological and pathological conditions. It promotes the orderly formation of new blood vessels by regulating endothelial cell (EC) proliferation, migration, and survival. The VEGF family consists of multiple ligands, among which VEGF-A is the most potent driver of angiogenesis. VEGF-A isoforms, generated through alternative splicing, exhibit distinct biological properties: VEGF-A165: the most abundant isoform with strong pro-angiogenic activity and heparin-binding capability VEGF-A121: highly diffusible but with relatively lower activity VEGF-A189: tightly binds to the extracellular matrix, forming localized concentration gradients VEGF-B and PlGF (Placental Growth Factor) primarily bind to VEGFR-1, contributing to metabolic regulation and pathological angiogenesis VEGF-C and VEGF-D are synthesized as precursors an...

The TP53 gene , also known as the p53 gene, is one of the most critical tumor suppressor genes in the human genome. Discovered in 1979 and recognized for its tumor-suppressive function in 1989, TP53 has since been regarded as the “guardian of the genome” and remains a central focus of cancer research. Under normal physiological conditions, the TP53 gene functions as a tightly regulated stress-response hub . The p53 protein encoded by the TP53 gene is constantly produced but also rapidly degraded. Upon DNA damage, replication stress, or metabolic imbalance, p53 becomes stabilized and activated, allowing it to orchestrate cell fate decisions. Rather than simply inducing apoptosis, p53 exerts a context-dependent regulatory role: In response to mild damage, p53 induces cell cycle arrest through transcriptional activation of targets such as p21, allowing time for DNA repair. Under moderate stress, p53 promotes DNA repair pathways and antioxidant responses. When damage is irreversible, ...

In a healthy state, cell growth, division, and death are precisely regulated. However, when key regulatory pathways malfunction, cells may escape this "command system," proliferating continuously and evading immune clearance, ultimately leading to disease—particularly tumors. As one of the world's leading malignancies, lung cancer has a complex pathogenesis rooted in the imbalance of cell growth regulatory systems. These imbalances are often genetic. For instance,  EGFR point mutations  allow the EGFR protein to activate automatically without the need for external ligand stimulation, magnifying downstream signals and leading to uncontrolled cell proliferation. EGFR is a receptor tyrosine kinase located on the cell membrane that regulates cell proliferation, differentiation, and survival across various tissues. Under normal conditions, when growth factors bind to EGFR, it triggers receptor dimerization and activates its kinase activity. This initiates a series of...