HO-2

Heme oxygenase-2 (HO-2) is a constitutively expressed enzyme that catalyzes the degradation of heme into biliverdin, carbon monoxide (CO), and free iron, playing a critical role in cellular antioxidant defense and cytoprotection^[1]. Unlike its inducible counterpart HO-1, HO-2 is primarily regulated at the transcriptional level and maintains baseline activity across various tissues, particularly in the brain, where it contributes to neuroprotection and modulation of oxidative stress^[2]. Emerging evidence highlights HO-2's involvement in regulating inflammation, apoptosis, and mitochondrial function, positioning it as a key modulator in pathophysiological conditions such as neurodegenerative diseases, cardiovascular disorders, and ischemia-reperfusion injury^[3]. In the central nervous system, HO-2 expression is tightly linked to neuronal survival and synaptic plasticity, with studies showing that HO-2 deficiency exacerbates neuronal damage following traumatic brain injury or stroke^[4]. Furthermore, CO released by HO-2 exerts anti-inflammatory and vasodilatory effects, suggesting therapeutic potential in inflammatory and vascular diseases^[5]. The dual roles of HO-2 in both protection and regulation of redox homeostasis underscore its significance as a molecular target for drug development. Despite its protective functions, excessive HO-2 activity may contribute to iron overload under pathological conditions, necessitating precise regulatory mechanisms^[6].