Lankenau Institute for Medical Research’s Post

In conclusion, we revealed that telomeres of endothelial cells implicated in coronary atherosclerosis were markedly shortened. This finding suggests that telomere shortening and replicative cellular senescence in coronary endothelial cells are focal phenomena and may play pathogenic roles in coronary atherogenesis and CAD. https://lnkd.in/gBqTH9Jc

In conclusion, we revealed that telomeres of endothelial cells implicated in coronary atherosclerosis were markedly shortened. This finding suggests that telomere shortening and replicative cellular senescence in coronary endothelial cells are focal phenomena and may play pathogenic roles in coronary atherogenesis and CAD. https://lnkd.in/gefif7QE

In conclusion, we revealed that telomeres of endothelial cells implicated in coronary atherosclerosis were markedly shortened. This finding suggests that telomere shortening and replicative cellular senescence in coronary endothelial cells are focal phenomena and may play pathogenic roles in coronary atherogenesis and CAD. https://lnkd.in/g3c_JyY7

Western blot for the weekend. Does Fisetin induce apoptosis of senescent vascular smooth muscle cells during cardiovascular aging ? Exposing the VSMCs to H2O2 to induce senescence ( a cellular aging hallmark ) via oxidative stress mechanisms then treat them with festin (flavonoid ) . Our pathway of interest is Pi3k-Akt-Bcl-2/Bcl-xl pathway… VSMCs with their phenotypic switching and proliferative capabilities play a significant role in cardiovascular dysfunction particularly atherosclerosis specifically during the fibrous cap formation. Our interest is to also show that Fisetin can restore proteostasis which , equally is another aging hallmark .. we try to find out ….

It's #FunFactFriday! 💡 Reactive Oxygen Species (ROS): friend or foe? 🤔 ROS are key cellular signaling molecules implicated in physiological processes. However, they also pose a serious threat to DNA integrity, and their accumulation has been associated with a number of pathological conditions. While ROS are often seen as the "bad guys", they can be harnessed for treating certain skin conditions and cancers using photodynamic therapy (PDT). In PDT, light-activated photosensitizer drugs are applied to generate ROS at a specific location within the body, effectively removing abnormal tissues. #metabolism #reactiveoxygenspecies #ROS #metaboliteassay #bioluminescence #promegatechnologies

Small molecule shows early-stage promise for repairing myelin sheath damage When treated with a novel protein function inhibitor called ESI1, mice that mimic the symptoms of multiple sclerosis (MS) and lab-prepared human brain cells both demonstrated the ability to regenerate vital myelin coatings that protect healthy axon function. This breakthrough, published in Cell, appears to overcome difficulties that have long frustrated previous attempts to reverse a form of nerve damage that robs people with MS of motor control and gradually blunts cognitive functions for many people as they age. “Currently, there are no effective therapies to reverse myelin damage in devastating demyelinating diseases such as MS,” says the corresponding author. “These findings are significant as they offer new pathways for treatment that potentially shift the therapeutic focus from just managing symptoms to actively promoting repair and regeneration of myelin.” #ScienceMission #sciencenewshighlights https://lnkd.in/ggvHDydR

What is the cause of mitochondrial dysfunction? Beginning at age 40, mitochondrial dysfunction naturally begins. "The most common cause of mitochondrial dysfunction is aging. There is an age-associated loss of mitochondrial cristae which would lead to decline in mitochondrial oxidative phosphorylation." ~ Dr. Hazel Szeto, creator of ReZilient (https://lnkd.in/gr95yzAV) Other causes for mitochondrial dysfunction is mitochondrial mutations, but these tend to be seen in young patients and chemotherapeutic agents. Source: https://lnkd.in/gUuwxGZk

Hyperphosphatemia is a complication of reduced kidney function in individuals with CKD and is associated with cardiovascular tissue calcification. Learn how researchers countered vascular calcification through mitochondrial phosphate transport inhibition in a murine model. http://ms.spr.ly/6045YpRo3

Here, Zhigang Li et al. show that myocardial infarction-induced cardiac damage and dysfunction in adult mice were reduced by overexpression of Adssl1 promoting cell cycle reentry and proliferation in cardiomyocytes. This effect was mimicked by treatment with inosine, a purine nucleoside whose amounts were increased by Adssl1 overexpression. Out in ScienceSignaling: https://lnkd.in/dQuHwnF7 Maybe potentiation of de novo purine synthesis could be a potential strategy to promote cardiac regeneration after insults to the heart.

remark:adenosine is a multifaceted molecule with multiple clinical uses due to its pharmacological properties and mechanism of action. Its ability to modulate cellular processes through specific receptor interactions makes it a valuable tool in treating a variety of medical conditions, from cardiac arrhythmias to respiratory diseases as well as potential neuroprotective applications. As research on adenosine continues, new clinical uses for this fascinating molecule may continue to emerge, further expanding its therapeutic potential in medicine. news url:https://lnkd.in/g3gGYSZY