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Comparative pathology and human disease
Human PATHOLOGY VOLUME 15
October 1984
NUMBER 10
Pathology Research Alert Comparative Pathology and Human Disease T h e pathogenesis of human diseases classified as chronic or degenerative poses major problems for the investigator, as exemplified by attempts to elucidate significant cardiovascular disorders. Atherosclerosis, valvular disease, and cardiomyopathy continue to challenge the ingenuity and resources of modern science. Countless animals have received artificial diets in attempts to induce atherosclerosis. Tile experimental production of rheumatic carditis and its complications remains to be accomplished. Induction of e x p e r i m e n t a l congestive heart failure usually requires surgical intervention and obstruction to flow. T h e scientific literature abounds in papers affirming that animal models do or do not simulate pathologic conditions in humans. T h e last two decades have demonstrated the importance of spontaneous animal disease to our understanding o f human disease. Spontaneotis means "naturally occurring," as distinguished from experimentally induced. Veterinary pathologists, working closely with human pathologists, have discovered significant areas of common interest. This cooperation has generated insights into mechanisms of disease, leading to innovative therapeutic strategies. T h e comparison o f similar diseases in animals and humans has been exceedingly useful in defining research questions with greater precision. Many of our new concepts in disease pathogenesis come directly from comparative pathology studies. No spontaneous animal models are available for certain diseases. However, advances in genetics and animal breeding may alter tile situation. Currently, spontaneous animal counterparts are being sought for such h u m a n diseases as i~heumatoid arthritis,
rheumatic valvular heart disease, noninfectious inflammatory bowel disease, and coronary atherosclerosis. A few years ago, hypertrophic and congestive cardiomyopathy was discovered in cats. Feline cardiomyopathy is now an important model for investigation. Following this discovery veterinarians in Taiwan reported the occurrence of spontaneous hypertrophic cardiomyopathy in swine. Researchers at the Pig Research Institute o f Taiwan control the breeding and diets of tile swine. If hypertrophic cardiomyopathy is related to genetic and dietary factors, tile implications for human disease are obvious. Most sought after has been a model of congestive heart failure in rodents. While heart failure occurs in cats with congestive cardiomyopathy and in dogs with mitral valvular fibrosis, there are too many areas of disimilarity with the h u m a n problem. Recently, a careful rat breeding program has apparently produced an animal with functional and structural manifestations of cardiomyopathy and congestive failure strikingly similar to those observed in humans. In a departure from established editorial policy, HUMAN PATHO1-OGV publishes in this issue a "Pathology Research Alert." We invited tile investigators to describe briefly their new rat model of an important human problem. This will alert human pathologists to the existence of the model and its potential for generating significant biologic data. T h e pathogenesis o f the failing heart and its structural representation have not been adequately understood in humans. With the a d v e n t of the rat spontaneous disease model, human pathologists can look forward to noteworthy advances that may shed some light on a vexing human disorder.---B.M.W.
901
October 1984
NUMBER 10
Pathology Research Alert Comparative Pathology and Human Disease T h e pathogenesis of human diseases classified as chronic or degenerative poses major problems for the investigator, as exemplified by attempts to elucidate significant cardiovascular disorders. Atherosclerosis, valvular disease, and cardiomyopathy continue to challenge the ingenuity and resources of modern science. Countless animals have received artificial diets in attempts to induce atherosclerosis. Tile experimental production of rheumatic carditis and its complications remains to be accomplished. Induction of e x p e r i m e n t a l congestive heart failure usually requires surgical intervention and obstruction to flow. T h e scientific literature abounds in papers affirming that animal models do or do not simulate pathologic conditions in humans. T h e last two decades have demonstrated the importance of spontaneous animal disease to our understanding o f human disease. Spontaneotis means "naturally occurring," as distinguished from experimentally induced. Veterinary pathologists, working closely with human pathologists, have discovered significant areas of common interest. This cooperation has generated insights into mechanisms of disease, leading to innovative therapeutic strategies. T h e comparison o f similar diseases in animals and humans has been exceedingly useful in defining research questions with greater precision. Many of our new concepts in disease pathogenesis come directly from comparative pathology studies. No spontaneous animal models are available for certain diseases. However, advances in genetics and animal breeding may alter tile situation. Currently, spontaneous animal counterparts are being sought for such h u m a n diseases as i~heumatoid arthritis,
rheumatic valvular heart disease, noninfectious inflammatory bowel disease, and coronary atherosclerosis. A few years ago, hypertrophic and congestive cardiomyopathy was discovered in cats. Feline cardiomyopathy is now an important model for investigation. Following this discovery veterinarians in Taiwan reported the occurrence of spontaneous hypertrophic cardiomyopathy in swine. Researchers at the Pig Research Institute o f Taiwan control the breeding and diets of tile swine. If hypertrophic cardiomyopathy is related to genetic and dietary factors, tile implications for human disease are obvious. Most sought after has been a model of congestive heart failure in rodents. While heart failure occurs in cats with congestive cardiomyopathy and in dogs with mitral valvular fibrosis, there are too many areas of disimilarity with the h u m a n problem. Recently, a careful rat breeding program has apparently produced an animal with functional and structural manifestations of cardiomyopathy and congestive failure strikingly similar to those observed in humans. In a departure from established editorial policy, HUMAN PATHO1-OGV publishes in this issue a "Pathology Research Alert." We invited tile investigators to describe briefly their new rat model of an important human problem. This will alert human pathologists to the existence of the model and its potential for generating significant biologic data. T h e pathogenesis o f the failing heart and its structural representation have not been adequately understood in humans. With the a d v e n t of the rat spontaneous disease model, human pathologists can look forward to noteworthy advances that may shed some light on a vexing human disorder.---B.M.W.
901