Researchers at the University of Texas at Arlington (UTA) have made significant strides in understanding how cells remove waste, a finding that could pave the way for improved treatments for autoimmune diseases and enhanced wound healing. Graduate student Alec Whited, in collaboration with doctoral student Aladin Elkhalil, discovered a previously unidentified cellular pathway that plays a crucial role in the clearance of dying cells. Their research was published in the journal Genetics in 2025.
Whited, who is currently a research assistant at UT Southwestern, explained that just as households need to regularly dispose of waste, living organisms must efficiently eliminate cells that are no longer needed. “This work helps us understand a specific step in the process of clearing those cells that have completed their job and are no longer needed,” he noted. “When this process is interrupted or does not work, it can cause major issues for the organism.”
Impact on Inflammation and Autoimmune Diseases
The study highlights the importance of clearing dying cells, particularly concerning inflammatory diseases. Whited indicated that the failure to effectively remove dead cells can trigger inflammation. When cells die, they release molecules that may be misinterpreted by the immune system as threats, potentially leading to chronic inflammation and contributing to conditions such as autoimmune diseases.
“This research underlines the necessity of maintaining cellular hygiene within the body,” Whited stated. “If these dead cells aren’t cleared out efficiently, the body may mistakenly interpret these molecules as threats and launch an immune response.”
Advancing Wound Healing Techniques
In addition to its implications for autoimmune diseases, the research offers insights into wound healing processes. One of the genes examined in the study is associated with cell-to-cell fusion, a vital mechanism in tissue repair. Whited expressed optimism about the potential applications of this knowledge. “By better understanding the genetic mechanisms behind this, we hope to identify additional genes that could play a role in improving wound healing,” he said.
The implications of this understanding could lead to advancements in treating chronic wounds, although Whited emphasized that further research is necessary to explore these connections fully.
Whited also shared his gratitude for the supportive research environment at UTA. He praised the collaborative spirit among faculty and students, which fosters academic growth and a sense of belonging within the scientific community. “The Department of Biology has been incredibly supportive,” he remarked. “This mindset fosters not only academic growth, but also a sense of belonging in the broader scientific community.”
As Whited continues his research journey, he remains committed to contributing significantly to the field. The findings presented in their study are not just a reflection of his individual efforts but a testament to the collaborative nature of scientific inquiry.
For more detailed insights, refer to Whited’s paper, titled “CDH-3/cadherin, YAP-1/YAP, and EGL-44/TEAD promote SYX-2/syntaxin and EFF-1 fusogen-mediated phagosome closure,” published in Genetics (2025). DOI: 10.1093/genetics/iyaf182.