Anissa Anindya Widjaja

The paper investigates the multi-layered repression system controlling C9ORF72 translation and identifies strategies to rescue loss-of-function in disease.

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.

This study identifies IL11's role in inhibiting LKB1/AMPK and activating mTOR through ERK/P90RSK, leading to metabolic dysfunction and fibrosis in multiple cell types and NASH in mice.

This study compares IL11 and IL11RA1 knockout mice, finding IL11 deficiency protects against lung fibro-inflammation but causes infertility, while IL11RA1 deficiency leads to craniosynostosis.

The paper investigates IL11-driven fibrosis mechanisms, showing ERK, not STAT3, drives fibrogenesis and identifies a novel role for nintedanib in inhibiting pro-fibrotic translation.

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.

The paper identifies translational regulators of fibrogenic genes in human cardiac fibroblasts and shows their role in cardiac fibrosis through ribosome profiling and RNA-binding protein analysis.

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.