FAK Family Kinases: A Potential Therapeutic Target for Atherosclerosis.
Xiuju GuanYue LiuYajuan AnXinshuang WangLiping WeiXin QiPublished in: Diabetes, metabolic syndrome and obesity : targets and therapy (2024)
Atherosclerosis (AS) is a chronic progressive inflammatory disease of the vascular wall and the primary pathological basis of cardiovascular and cerebrovascular disease. Focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), two highly homologous members of the FAK family kinases, play critical roles in integrin signaling. They also serve as scaffolding proteins that contribute to the assembly of cellular signaling complexes that regulate cell survival, cell cycle progression, and cell motility. Research indicates that the FAK family kinases is involved in the gene regulation of vascular cells and that aberrant expression of this family is associated with pathological changes in vascular disease. These findings establish the FAK family kinases as a critical signaling mediator in atherosclerotic lesions and inhibition of its activity has the potential to attenuate the pathological progression of AS. This review highlights the indispensable role of the FAK family kinases in abnormal vascular smooth muscle cell proliferation, endothelial cell dysfunction, inflammation, and lipid metabolism associated with AS. We also summarize therapeutic targets against the FAK family kinases, providing valuable insights into therapeutic strategies for AS.
Keyphrases
- cell cycle
- cell migration
- tyrosine kinase
- cell proliferation
- smooth muscle
- oxidative stress
- cardiovascular disease
- type diabetes
- dna damage
- stem cells
- epidermal growth factor receptor
- poor prognosis
- induced apoptosis
- escherichia coli
- signaling pathway
- cell death
- risk assessment
- single cell
- long non coding rna
- staphylococcus aureus
- biofilm formation
- dna repair
- pi k akt
- endoplasmic reticulum stress