Interferon and heart disease.

Heart disease is the leading cause of morbidity and mortality in the United States. Atherosclerosis is the major cause of heart disease. It is a chronic inflammatory response.

Chronic obstructive pulmonary disease and cytokines.

Chronic obstructive pulmonary disease is a leading cause of morbidity and mortality. Understanding what happens at a cellular level will lead to more effective treatments. Interleukins and transforming growth factor-beta are important inflammatory mediators that may be significant in the evolution of chronic obstructive pulmonary disease.

C-reactive protein, stroke, and statins.

C-reactive protein (CRP) is an important indicator and player in inflammatory diseases such as stroke. It may be involved in the earliest stages of stroke. Monitoring the levels of CRP may help in the prevention and treatment of stroke.

Endothelin-1-mediated inflammation in acute renal failure.

Acute renal failure presents a serious and life-threatening problem in hospitalized patients. Current therapies address the systemic alterations in renal failure. Cellular changes also occur.

The role of endothelin in heart failure.

Current treatments for heart failure extend the life of the patient but do not stop the progression of the disease process. These treatments may not be addressing the underlying cause of cellular injury. The role of endothelin in cardiac remodeling and inflammation may be important in the progression of failure, and endothelin antagonists may be beneficial in treatment in combination with drugs already in use.

Inflammatory bowel disease and endothelin-1: a review.

Inflammatory bowel disease (IBD) appears to be an inappropriate response to an antigen that leads to chronic inflammation rather than repair. This review looks at the role of endothelin-1 (ET-1) as a proinflammatory agent in IBD. ET-1 antagonists in animal models reduce the incidence and severity of IBD.

Sickle cell crisis and endothelin antagonists.

Sickle cell crisis may be more complex than a vaso-occlusive event in response to hypoxia. Endothelin-1 (ET-1) is a potent vasoconstrictor and mitogen secreted in response to hypoxia. ET-1 contributes to the vaso-occlusion and inflammation in sickle cell crisis.

Thromboembolic disease and cancer: possible new treatments.

Hypoxia-induced endothelin (ET) and vascular endothelial growth or permeability factor (VEGF) play an important role in tumor biology by promoting angiogenesis. Angiogenesis alters hemostasis and promotes thromboembolic disease (TED). Therapeutic angiogenesis directed against ET and VEGF may reduce the incidence of TED in cancer patients.