A recent review in Current Molecular Pharmacology explores the mechanisms and treatments for hepatic ischemia-reperfusion injury (IRI), a major cause of liver dysfunction post-transplant. The study highlights antioxidant therapies, surgical techniques, and pharmacological interventions, emphasizing the potential of compounds like N-acetylcysteine and ornithine. "Targeting oxidative stress and inflammation is key," said lead author Kuldeep Singh.

A comprehensive review by researchers at Taylor’s University highlights the oncogenic role of mutant p53 (mutp53) in cancer progression and resistance to therapy. The study explores preclinical and clinical advancements in mutp53-targeting compounds, with APR-246 leading the charge in Phase III trials. These inhibitors aim to restore wild-type p53 function, offering new hope for precision cancer treatment.

A study led by Yubo Xu at Tongji University reveals that Fangchinoline (Fan), a compound from Stephania tetrandra, triggers oxidative stress-induced DNA damage and apoptosis in Jurkat T cells while inhibiting Akt signaling. This dual mechanism highlights Fan’s potential as a therapeutic agent for Sjögren’s syndrome (SS), where T cell infiltration drives disease progression.

A comprehensive review in Current Molecular Pharmacology explores sarcopenia’s molecular pathways and cutting-edge interventions. Led by Priyanka Prajapati and team, the study highlights oxidative stress, mitochondrial dysfunction, and promising treatments like exercise, nutraceuticals, and hormone therapy. "Targeting these pathways could revolutionize sarcopenia management," said Prajapati.

A groundbreaking study in Current Molecular Pharmacology uncovers how deeply quiescent leukemia stem cells (LSCs) in chronic myeloid leukemia (CML) evade therapy by suppressing mitochondrial complex I (MC-1) and relying on fatty acid oxidation (FAO). Led by Dr. Nyam-Osor Chimge and Dr. Michael Kahn, the research identifies the CBP/β-catenin antagonist ICG-001 as a potential strategy to force differentiation and eliminate resistant cells. "Targeting this metabolic vulnerability could revolutionize CML treatment," said Dr. Kahn.