I see that laminar stress and oscillatory shear stress include the topics of senescence, autophagy, and STING.
Oscillatory shear stress promotes atherosclerosis via inducing STING activation. Activation of STING pathway induces endothelial cell senescence in atherosclerosis. Oscillatory shear stress mediating STING activation via mitochondrial DNA leakage.
In this study, we found that laminar shear stress(LSS) could inhibit the increased expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase-9 (MMP-9) caused by TNF-α in an autophagy-dependent pathway in human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Whole-transcriptome sequencing analysis revealed that erythropoietin-producing hepatocyte receptor B2 (EPHB2) was a key gene in response to LSS. Moreover, co-immunoprecipitation assay indicated that LSS could enhance the EPHB2-mediated nuclear translocation of high mobility group box-1 (HMGB1), which interacts with Beclin-1 (BECN1) and finally leads to autophagy.
This tangent is interesting.
Oh, it's not a tangent! Senescence may be part of the vicious cycle.
pmc.ncbi.nlm.nih.gov
Oscillatory shear stress promotes atherosclerosis via inducing STING activation. Activation of STING pathway induces endothelial cell senescence in atherosclerosis. Oscillatory shear stress mediating STING activation via mitochondrial DNA leakage.
In this study, we found that laminar shear stress(LSS) could inhibit the increased expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase-9 (MMP-9) caused by TNF-α in an autophagy-dependent pathway in human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Whole-transcriptome sequencing analysis revealed that erythropoietin-producing hepatocyte receptor B2 (EPHB2) was a key gene in response to LSS. Moreover, co-immunoprecipitation assay indicated that LSS could enhance the EPHB2-mediated nuclear translocation of high mobility group box-1 (HMGB1), which interacts with Beclin-1 (BECN1) and finally leads to autophagy.
This tangent is interesting.
Oh, it's not a tangent! Senescence may be part of the vicious cycle.
Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS
Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS - PMC
Vascular aging is associated with the development of cardiovascular complications, in which endothelial cell senescence (ES) may play a critical role. Nitric oxide (NO) prevents human ES through inhibition of oxidative stress, and inflammatory ...
pmc.ncbi.nlm.nih.gov
