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Heme oxygenase (HO) exists as constitutive (HO-2, HO-3) and inducible isoforms (HO-1), the latter which responds to regulation by multiple stress-stimuli [1]. Several signaling molecules (e.g., mitogen-activated protein kinases), transcriptional regulators (activator protein-1, NF-E2-related factor-2, hypoxia-inducible factor-1, Bach-1), as well as two enhancer regions in the ho-1 5' regulatory region, participate in the regulation of the ho-1 gene [2]. Recent progress indicates that carbon monoxide (CO), a gaseous second messenger, exerts novel anti-inflammatory and anti-apoptotic effects (Table 1), although little is known about the precise molecular mechanism of these actions. There has been many reports that inhalation of CO could be protective against acute ischemia-reperfusion injury in intestine, lung, kidney, and liver (Table 2). More recent report indicates that inhalation of 100–125 ppm CO by patients with chronic obstructive pulmonary disease is feasible and leads to trends in reduction of sputum eosinophils and improvement of responsiveness to methacholine [3]. In addition to beneficial effects of CO, further studies need to confirm the safety of this gas, especially in the cardiac function [4, 5]. In this serial review, we invited several outstanding researchers in this field to summarize their work, to review their peers’ activity, and to encourage us their opinions. I thank all the anonymous reviewers of these articles for their insightful comments.    Table 1  Mechanisms of anti-inflammatory and cytoprotective effects of carbon monoxide      Table 2  Effects of inhalated carbon monoxide on experimental disease models in rodents

Introduction to Serial Review: Heme Oxygenase and Carbon Monoxide: Medicinal Chemistry and Biological Effects