**1. Introduction**

Atherosclerosis is a disease that belongs to both antiquity and modern era [1]. This economi‐ cally important disease is an outcome of both genetic and environmental risk factors and their interactions [2]. Inflammatory and metabolic derangements and their synergy are the main

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causes in the etiopathogenesis of atherosclerosis [3]. However, all aspects of atherosclerosis are not known at the present time, and more human and animal studies are requested to decode the black box of atherosclerosis. Since we are not able to do interventional studies in humans, animal models are good simulated and translated tools in this endeavor.

Many seminal reviews (e.g., see [4–6]) have shown that rabbits are good, reliable, and cheap animal models of atherosclerosis, with a high degree of comparability to human's atheroscle‐ rosis. In this context, low-density lipoprotein cholesterol (LDL-C) is predominant plasma lipoprotein in rabbits and humans [6].

Despite these data, the amount of dietary cholesterol, the diet formula, and the duration of cholesterol feeding necessary to induce translated atherosclerosis are not conclusive among experimental studies (e.g., see [7,8]). In this line, Prof. Watanabe and colleagues [9] partially solved this problem by producing a genetic rabbit model of hypercholesterolemia many years ago. However, this expensive model is not globally available in all laboratories and is not suitable for translating nutritional interventions that lead to atherosclerosis. Watanabe rabbit is still not a pet animal model for studying atherosclerosis in all laboratories.

In addition, there is not any concert about the methodology used for inducing atherosclerosis in nongenetic animal models like New Zealand rabbits (NZRs) among various studies. In this sense, reliable and loyal translation of atherosclerosis in rabbits were hampered by methodo‐ logical limitations, including suitable sample size, suboptimal biomarker assay, amount of cholesterol intake, routes of cholesterol intake, and duration of cholesterol intake, among others. The aforementioned limitations result in low statistical power to translate atheroscle‐ rosis in animal models like rabbits.

To obtain a more truthful and defined estimation of association between cholesterol intake and atherosclerosis (i.e., the occurrence of dyslipidemia), to do root cause analysis, and to explore the source of heterogeneity among randomized controlled trials (RCTs), we conducted a metaanalysis of RCTs by evaluating the associations of dietary cholesterol with the dyslipidemia component of atherosclerosis in rabbits.
