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Isoproterenol-induced cardiac hypertrophy is a well-established experimental model that mimics environmental stress exposure and the pathological consequences of chronic sympathetic overstimulation on the heart. This model suggests critical understanding in to molecular and cellular mechanisms underlying maladaptive cardiac remodeling, a precursor to heart failure. At the mechanistic level, isoproterenol-induced cardiac hypertrophy is driven by multiple interconnected signaling pathways and triggered by sustained mechanical load, neurohormonal stimulation, inflammatory responses and environmental stressors, that often preceding fibrosis, ventricular dysfunction, and heart failure. Concurrently, excessive production of reactive oxygen species (ROS) generates oxidative stress, which damages cellular macromolecules and disrupts functions of cellular organelles. Inflammatory responses are also triggered, largely mediated by transcription factors such as the NF-kB pathway, resulting in the upregulation of pro-inflammatory cytokines and profibrotic factors. Additional signaling cascades, including the MAPK pathway, further amplify hypertrophic gene expression and cardiac remodeling. Environmental stressors like chronic psychological stress, air pollution, thermal strain and unhealthy lifestyle habits tend to trigger overlapping neurohormonal and molecular responses. These effects closely resemble those seen in Isoproterenol-induced cardiac hypertrophy models. Such conditions lead to prolonged sympathetic stimulations, increased oxidative stress and persistent-low grade inflammation, all of which contribute to the onset and progression of cardiac hypertrophy which makes Isoproterenol-induced cardiac injury often used as a practical model to study cardiovascular damage driven by environmental factors. Current molecular cardioprotective strategies largely target oxidative stress and inflammatory pathways. In this context, enhancing endogenous antioxidant defence mechanisms particularly through activation of Nrf2 pathway has gained attention as an effective means to limit ROS-mediated damage. Pharmacological interventions such as β-blockers and angiotensin-converting enzyme inhibitors help to reduce β-adrenergic overstimulation and are known to improve cardiac outcomes. In contrast, naturally derived bioactive compounds including polyphenols and flavonoids have demonstrated significant antioxidant and anti-inflammatory potential thereby attenuating hypertrophic signaling and preserving myocardial structure and function. Therefore, this review focuses on Isoproterenol-induced cardiac hypertrophy as an experimental model to examine the interplay between neurohormonal activation, environmental stressors and the molecular mechanisms underlying cardiac remodeling. A clearer understanding of these interconnected pathways is expected to not only provide insight into disease progression but also support the development of more targeted cardioprotective strategies aimed at reducing the global burden of cardiovascular disease.