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Background and Aims NAFLD represents an increasing health problem in association with obesity and diabetes with no effective pharmacotherapies. Growing evidence suggests that several FGFs play important roles in diverse aspects of liver pathophysiology. Here, we report a previously unappreciated role of FGF4 in the liver. Approach and Results Expression of hepatic FGF4 is inversely associated with NAFLD pathological grades in both human patients and mouse models. Loss of hepatic Fgf4 aggravates hepatic steatosis and liver damage resulted from an obesogenic high‐fat diet. By contrast, pharmacological administration of recombinant FGF4 mitigates hepatic steatosis, inflammation, liver damage, and fibrogenic markers in mouse livers induced to develop NAFLD and NASH under dietary challenges. Such beneficial effects of FGF4 are mediated predominantly by activating hepatic FGF receptor (FGFR) 4, which activates a downstream Ca2+–Ca2+/calmodulin‐dependent protein kinase kinase beta–dependent AMP‐activated protein kinase (AMPK)‐Caspase 6 signal axis, leading to enhanced fatty acid oxidation, reduced hepatocellular apoptosis, and mitigation of liver damage. Conclusions Our study identifies FGF4 as a stress‐responsive regulator of liver pathophysiology that acts through an FGFR4‐AMPK‐Caspase 6 signal pathway, shedding light on strategies for treating NAFLD and associated liver pathologies.

Electronic defects and grain boundaries of perovskite films will significantly deteriorate both the efficiency and the stability of perovskite solar cells (PSCs), and various methods aimed to reduce these defects are proposed. Herein, an organic solid molecule of pyridinedicarboxylic acid (PDA) with one pyridine and two carboxylic acid groups is used as a passivating agent to cure the defects by regulating the perovskite microstructures in a multiple manner. The defects located at both the surfaces and grain boundaries of polycrystalline MAPbI3 perovskites are simultaneously passivated through the multiple coordination effects between the used functional groups and uncoordinated Pb2+, regardless of the substitution sites of the carboxylic acid and pyridine. Impressively, the PDA‐passivated inverted PSCs achieve remarkably enhanced power conversion efficiencies (PCEs) from 16.43% to nearly 19% and maintain over 90% of its original PCE after 1300 h under an inert environment. These findings indicate that the commercially available PDA molecule emerges as an efficient passivating agent of perovskite defects capable of stimulating the combined effects of the multiple functional groups, which is highly promising for the practical applications of PSCs with both high efficiency and good stability.

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