A new scientific study conducted by King Abdullah University of Science and Technology (KAUST) has revealed that restoring a key cellular molecule involved in energy production may partially reverse the harmful effects caused by acidic stress in human cells.
Published in Communications Biology, the research explored how human cells react to mildly acidic environments — conditions commonly found in tumors, chronic inflammation, and aging organs — yet whose direct cellular effects remain insufficiently understood.
KAUST Associate Professor of Bioscience Mo Li explained that the research relied on a highly controlled bioreactor system, allowing scientists to directly observe how mild acidity affects cellular behavior.
The findings showed that even slight increases in acidity can significantly disrupt the way cells generate energy, impair mitochondrial performance, and activate cellular stress responses.
Li added that supplementing cells with a molecule widely associated with longevity research was able to partially restore metabolic activity and improve overall cellular health under acidic conditions.
Researchers emphasized that these findings are particularly important because similar acidic environments occur in diseases such as cancer and chronic inflammation, potentially helping scientists develop future strategies aimed at protecting cells and supporting human health.
According to KAUST, tissue acidity has long been recognized as a characteristic of several diseases, but the direct biological impact on human cells has remained unclear due to limitations in experimental precision.
During the study, scientists used a tightly controlled experimental system to isolate the effects of pH levels from other influencing factors, providing a clearer understanding of the biological changes occurring within cells.
Postdoctoral researcher Yingzi Zhang explained that the team developed a new multi-omics research framework linking acidity to metabolic reprogramming, immune system activation, and instability in the mitochondrial genome, supported by advanced metabolomics, transcriptomics, and epigenomics data.
