dc.description.abstract | Hypertension is one predictive factor for stroke and heart ischemic disease. Nowadays,
it is considered an inflammatory disease with elevated cytokine levels, oxidative
stress, and infiltration of immune cells in several organs including heart, kidney,
and vessels, which contribute to the hypertension-associated cardiovascular damage.
Macrophages, the most abundant immune cells in tissues, have a high degree of
plasticity that is manifested by polarization in different phenotypes, with the most
well-known being M1 (proinflammatory) and M2 (anti-inflammatory). In hypertension,
M1 phenotype predominates, producing inflammatory cytokines and oxidative stress,
and mediating many mechanisms involved in the pathogenesis of this disease. The
increase in the renin–angiotensin system and sympathetic activity contributes to the
macrophage mobilization and to its polarization to the pro-inflammatory phenotype.
Heme oxygenase-1 (HO-1), a phase II detoxification enzyme responsible for heme
catabolism, is induced by oxidative stress, among others. HO-1 has been shown to
protect against oxidative and inflammatory insults in hypertension, reducing end organ
damage and blood pressure, not only by its expression at the vascular level, but also
by shifting macrophages toward the anti-inflammatory phenotype. The regulatory role
of heme availability for the synthesis of enzymes involved in hypertension development,
such as cyclooxygenase or nitric oxide synthase, seems to be responsible for many of
the beneficial HO-1 effects; additionally, the antioxidant, anti-inflammatory, antiapoptotic,
and antiproliferative effects of the end products of its reaction, carbon monoxide,
biliverdin/bilirubin, and Fe2C, would also contribute. In this review, we analyze the role
of HO-1 in hypertensive pathology, focusing on its expression in macrophages. | es |