Cellular Stress Responses
It is currently understood that a pathological stress response is a hallmark of many common human diseases for a number of reasons. Firstly, the stress stimulus may be too strong and/or prolonged, thereby allowing insufficient time for recovery to the normal status.
This review summarized mitochondrial functions in cardiovascular system under physiological mechanical stress and mitochondrial dysfunction under pathological mechanical stress in CVDs (graphical abstract).

It is currently understood that a pathological stress response is a hallmark of many common human diseases for a number of reasons. Firstly, the stress stimulus may be too strong and/or prolonged, thereby allowing insufficient time for recovery to the normal status.
Importantly, the mobilization of stress responses in pathological conditions supports the use of laboratory animal stress models to understand pathways and mechanisms controlling responses measured (but not the disease itself).

Furthermore, visual representations like the one above help us fully grasp the concept of Under Pathological Stress.
These pathological conditions result in development of residual urine, resulting in bladder wall stretching. Thus, stretching could be a common causative factor.
Understanding Under Pathological Stress Before the Gallery
Schematic working hypothesis. Under pathological stress, myocardial Ang. For Under Pathological Stress, this point helps readers notice the most relevant visual details before moving into the gallery.
UPR Activation in Following Experimental vs. Pathological Stress. It works as a short bridge between the article summary and the gallery section.
Role of PQC systems in cardiac function under pathological stress. The extra context helps the page feel more useful without forcing the same phrase repeatedly.
Looking at multiple sources also helps separate the main idea from small decorative details.
These notes are added so the page offers more than images and gives each visitor a clearer reason to keep reading.