Rui Wang (Editor).
Boca Raton, Fl: CRC, 2002, 320 pp., illus., index, $129.95
ISBN: 0-8493-1041-5
This book contains fifteen chapters by investigators who have contributed data that support the concept that there are effects of endogenously produced carbon monoxide on cardiovascular function. It is a by-product of an international symposium and the emphasis in most of the chapters is on research performed by the authors. In general, topics are restricted to possible carbon monoxide signaling in the cardiovascular system, emphasizing heme oxygenase (HO)-catalyzed formation of carbon monoxide and how this may activate soluble guanylyl cyclase or modulate cytochrome P-450 or Kv, KCa2+ and KATP channels. There are chapters that review possible roles of HO-1- and/or carbon monoxide-mediated signal transduction in patients with hypertension, diabetes, cardiac dysfunction states, cardiovascular inflammation, and ischemic heart damage. There is an interesting description of a single human patient that had HO-1 deficiency, but it is not clear if pathophysiology was due to lack of carbon monoxide signaling or an effect of HO-1 deficiency independent of its role in producing endogenous carbon monoxide.
A major value of this volume is that the reader obtains a sense of an active area of research and the tools that are currently being used in this research. The book is most worthwhile for people interested in details of multiple investigations reviewed here. However, individual chapters add little that wasn't addressed in previously communications written by the authors who contributed to this book. There is considerable redundancy in different chapters, the quality of the presentations is variable and an overview of the field is not well developed. Because the authors consider only cardiovascular investigations, contributions of workers who made seminal early observations that drove the field of carbon monoxide signaling are largely ignored. It would have been useful to include a chapter devoted to whether or not carbon monoxide formed via HO-catalyzed heme degradation is involved in signal transduction, reviewing data obtained in different tissues and preparations, the limitations of the database, and how this cascade might operate. Because of HO’s important role as a key component of the carbon monoxide signaling system, it would be pertinent to include an in depth discussion of what is known about HO isoforms, including putative activation and inactivation mechanisms and control of substrate availability. One looks but does not find a critical discussion of the assumption that cellular effects of experimentally altering HO-1 content are due to effects on CO-mediated signal transduction. Because of the parallelism between nitric oxide-, carbon monoxide-, hypoxia- and hyperoxia-induced signaling, this reviewer would have liked to see an in-depth comparison of these signaling systems (there is a chapter devoted to nitric oxide and carbon monoxide signaling but it could be considerably expanded on). There is no considerations of temporal or spatial aspects of carbon monoxide signaling or how this putative mediator is degraded or excreted. In conclusion: this book brings together multiple studies of different areas of carbon monoxide signaling in cardiovascular tissue which could be valuable to investigators, but lacks broad and critical discussion.
Ronald F. Coburn
University of Pennsylvania
School of Medicine
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