The etiology of liver cirrhosis has transformed from hepatitis B virus-driven to metabolic dysfunction-associated steatotic liver disease (MASLD). In this context, researchers have compared the viral and metabolic cirrhosis, highlighting the differences in their key pathogenic mechanisms and the limited applicability of viral therapeutic strategies for treatment of MASLD. This necessitates the development of new strategies for diagnosis and treatment of MASLD.

NTU Singapore scientists have identified a fat-producing enzyme (GPAT) in brain cells that amplifies the damage caused by α-synuclein, the protein linked to Parkinson's disease. GPAT delivers a "double hit" — impairing cells' energy-producing machinery while increasing the protein's toxicity. Reducing GPAT activity led to less brain cell damage in lab models. The findings point to a potential new treatment target for a disease that currently has no cure.

A study published in Cell Research [https://doi.org/10.1038/s41422-026-01245-5] advances a central idea in stem cell biology by identifying a checkpoint that controls the identity of many different types of stem cells across developmental stages.

For nearly two decades, scientists have understood that stem cell self-renewal depends on blocking differentiation signals—a concept described in earlier work, including Qi-Long Ying and Austin Smith’s 2008 Nature paper “The ground state of embryonic stem cell self-renewal.”

Now, researchers from the labs of Ying at USC and Guang Hu at the National Institute of Environmental Health Sciences (NIEHS), one of the National Institutes of Health (NIH), have identified the protein GSK3α as a “stemness checkpoint” that drives differentiation and that can be inhibited to maintain stem cell identity.

This discovery introduces a new conceptual framework: rather than viewing stem cell maintenance as the result of many unrelated signaling conditions, distinct stem cell types share common checkpoints.