Abstract: Hypertensive emergency (HE) is a clinical syndrome marked by a rapid increase in blood pressure, which is often accompanied by progressive organ damage. Traditional treatment primarily aims to reduce blood pressure but fails to effectively halt the progression of injury. This article introduces a core pathophysiological framework known as the "endothelium-mitochondria-inflammation immune axis (EMIIA)." This paper proposes a core pathophysiological framework termed the "endothelium-mitochondria-inflammatory immune axis", with a focus on analyzing: acute pressure overload-mediated endothelial mechanical injury and dysfunction; mitochondrial oxidative stress and energy metabolism disorders; ectopic distribution of mitochondrial DNA (mtDNA) triggering the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING)-NOD-like receptor family pyrin domain containing 3 (NLRP3)-nuclear factor kappa-B (NF-κB) cascade, which initiates an immuno-inflammatory response; and microcirculatory injury characterized by pyroptosis. The article suggests that targeted endothelial protection, the maintenance of mitochondrial homeostasis, and the regulation of inflammatory signals represent promising therapeutic avenues. Furthermore, multi-dimensional biomarkers serve as a basis for stratifying early-stage high-risk patients. This systematic review aims to elucidate the pathway from mechanistic research to precise clinical intervention, with the hope of providing new insights for developing individualized prevention and treatment strategies for HE.