Wei‐Wen Lim

This study identifies ST2-expressing fibroblasts as drivers of Peutz-Jeghers syndrome polyposis and shows IL-11 as a therapeutic target.

This paper identifies direct cardiomyocyte toxicities of IL11 therapy, showing it causes acute heart failure by activating JAK/STAT3, which questions its continued use in patients.

This study shows that IL11 expression in cardiomyocytes causes cardiac fibrosis, inflammation, and dysfunction, contradicting previous reports of its anti-fibrotic effects.

This study shows that inhibiting IL11 improves healthspan in aged mice by reversing metabolic dysfunction, sarcopenia, and frailty.

This study shows IL11 promotes inflammation in fibroblasts by upregulating IL33 and other proinflammatory genes, with STAT3 signaling being critical for this effect.

The paper shows that autocrine IL11 signaling in hepatocytes drives lipotoxicity and NASH by causing lipoapoptosis and reactive oxygen species, with protection seen in Il11ra1-deleted mice.

The paper identifies IL-11 as a therapeutic target in idiopathic pulmonary fibrosis by showing its role in fibroblast activation and fibrosis progression across species.

This study identifies IL-11 as a key driver of HSC-to-myofibroblast transformation in NASH, showing that targeting IL-11 reduces fibrosis and inflammation in preclinical models.