Chapters authored
Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome
The National Heart, Lung, and Blood Institute Working Group has postulated the cardiorenal syndrome (CRS) as an interaction between the kidneys and the cardiovascular system in which therapy to relieve congestive heart failure (HF) symptoms is limited by the further worsening renal function. CRS is classified from type I to V, taking into account the progression of the symptoms in terms of mechanisms, clinical conditions, and biomarkers. Experimental and clinical studies have shown the kidney as both a trigger and a target to sympathetic nervous system (SNS) overactivity. Renal damage and ischemia, activation of the renin angiotensin aldosterone system (RAAS), and dysfunction of nitric oxide (NO) system are associated with kidney adrenergic activation. Indeed, the imbalances of RAAS and/or SNS share an important common process in CRS: the activation and production of free radicals, especially reactive oxygen species (ROS). The present chapter addresses connections of the free radicals as potential biomarkers as the imbalances in the RAAS and the SNS are developed. Understanding the involvement of free radicals in CRS may bring knowledge to design studies in order to develop accurate pharmacological interventions.
Part of the book: Free Radicals and Diseases
Signaling Pathways of Cardiac Remodeling Related to Angiotensin II
Heart failure affects more than 23 million people worldwide, and its prognosis remains poor. Hypertension is one of the most prominent human health problem and places individuals at a higher risk for heart failure. Several factors interplay the development of hypertension contributing for decompensated heart hypertrophy. The renin-angiotensin system (RAS) has been shown to be the foremost regulator of blood pressure. Many evidences have pointed out the importance of RAS and its key mediator, angiotensin II (Ang II), on signaling pathways involved in cardiac remodeling. The Ang II-induced hypertrophic effects seem to be related to increased reactive oxygen species (ROS). Under oxidative stress conditions, as those observed in hypertension and heart failure, the matrix metalloproteinases (MMP) is activated. Ang II is connected with TNF-α and TGF-β by ROS-NF-κB-MMP mechanisms, which are involved in heart failure. The rationale of the present chapter is structured on the progression of heart failure related to Ang II, TNF-α and TGF-β by common signaling pathways. Pharmacotherapeutics approaches to the heart failure abound, but the mortality rates remain high. This chapter will also describe molecular mechanisms involved in heart failure highlighting that TGF-β and/or TNF-α inhibitors could contribute to treatment to this serious clinical condition.
Part of the book: Renin-Angiotensin System