The Science & Technology desk gathers a weekly digest with impactful and interesting research publications and developments at Stanford. Read the latest in this week’s Research Roundup.
Visualizing “zombie cells”
In a paper published in npj Imaging, a team of Stanford and Northwestern researchers found an MRI agent that helps visualize dormant “zombie” cells that contribute to osteoarthritis.
Over 30 million adults in the U.S. have osteoarthritis, a condition that weakens the cartilage between joints. While different factors can contribute to osteoarthritis, senescent cells — “zombie” cells that are still alive but non-functioning — are particularly significant. Although dormant, these deceiving cells secrete molecules that can negatively impact surrounding tissue. As the number of senescent cells generally increases with age, osteoarthritis can consequently develop or worsen.
While senolytic therapies — therapies that target these senescent cells — currently exist, there was previously no way to properly visualize the cells. Now that researchers have developed a system to do so, they are not only able to light up these cells to visualize them but also track the progress and efficacy of therapies.
The scientists selected gadolinium, an MRI agent that illuminates all tissues. However, to selectively target senescent cells, they added a “cage” around the agent which would only open when encountering a specific protein.
After this study, the scientists are even more hopeful; Heike Daldrup-Link, professor of radiology, highlighted that the MRI can provide information about a patient’s potential state of arthritis much faster than current methods.
“We envision that our contrast agent could fill this gap,” Daldrup-Link told Stanford Medicine, referring to the fact that current clinical trials tracking patients’ symptoms require significant time.
A new way to treat cardiac fibrosis
In a Stanford-led study published in Nature, researchers detailed a new strategy to beat cardiac fibrosis, a condition with no current treatment that is characterized by scarring of the heart tissue. Cardiac fibrosis impairs contractility of the heart muscle cells, increasing the risk of a heart attack.
Through multiple rounds of sequencing, the researchers first identified SRC, a protein that is significantly activated in diseased hearts. They then screened for compounds that could inhibit this protein, deciding saracatinib, a compound that was previously used in cancer research.
A series of experiments with saracatinib revealed that it lowers the impact of fibrosis, especially when combined with the suppression of another pathway that is responsible for fibroblast activation. Contractile function – movement through the use of proteins – of the heart muscle cells was also restored.
Joseph Wu, senior author of the study and director of the Stanford Cardiovascular Institute, explained that this new strategy will not come at the expense of other cells with fundamentally important functions.
“We want to break this vicious cycle – but until now, there’s been no reliable way to do so selectively in fibroblasts without affecting other essential heart cell types, such as cardiomyocytes,” Wang told Stanford Medicine.