Genetically modified mammalian circadian clock models

This supplemental table is a curated literature table summarizing reported metabolic, cardiovascular, inflammatory, and mitochondrial phenotypes associated with genetic manipulation of circadian clock genes in experimental rodent models. It is linked to the review by Sato, Alammar et al. “Tick Tock: How the Body’s Circadian Clock Keeps Cardiometabolic Rhythm in Check”. The table focuses primarily on BMAL1 (Bmal1/Arntl) and also includes CLOCK, CRY1, CRY2, PER1, PER2, PER3, NR1D1, NR1D2, NFIL3, NPAS2 and RORa perturbations. For each study, the dataset records the targeted gene, genetic manipulation (e.g., knockout, knockdown, overexpression, mutation, and/or rescue), affected organ or cell type, and reported effects, where available, on body weight/obesity, glucose homeostasis, insulin or leptin signaling, lipid metabolism, inflammation/immunity, atherosclerosis and vascular function, blood pressure, cardiac function, mitochondrial activity, thermogenesis, and energy expenditure. Where available, sex-specific findings, PubMed identifiers (PMIDs), and full study citations are provided. The dataset is intended to facilitate systematic comparison of how disruption or modification of circadian clock components influences metabolic and cardiovascular physiology across tissues and experimental models. It may be useful for literature reviews, hypothesis generation, identification of tissue-specific effects, and analysis of relationships between circadian regulation and metabolic or cardiovascular disease. The table represents findings reported in the cited publications and should be interpreted in the context of the experimental conditions, genetic models, tissues, and interventions used in each individual study. We acknowledge that, despite our efforts, some relevant papers may not have been included.