Kumuda C Das1, Venkatesh Kundumani-Sridharan2, Jaganathan Subramani2. 1. Department of Translational and Vascular Biology, University of Texas Health Sciences Center at Tyler, 11937 US Hwy 271, Tyler, TX, 75708, USA. Kumuda.das2@uthct.edu. 2. Department of Translational and Vascular Biology, University of Texas Health Sciences Center at Tyler, 11937 US Hwy 271, Tyler, TX, 75708, USA.
Abstract
PURPOSE OF REVIEW: Although the roles of oxidant stress and redox perturbations in hypertension have been the subject of several reviews, role of thioredoxin (Trx), a major cellular redox protein in age-related hypertension remains inadequately reviewed. The purpose of this review is to bring readers up-to-date with current understanding of the role of thioredoxin in age-related hypertension. RECENT FINDINGS: Age-related hypertension is a major underlying cause of several cardiovascular disorders, and therefore, intensive management of blood pressure is indicated in most patients with cardiovascular complications. Recent studies have shown that age-related hypertension was reversed and remained lowered for a prolonged period in mice with higher levels of human Trx (Trx-Tg). Additionally, injection of human recombinant Trx (rhTrx) decreased hypertension in aged wild-type mice that lasted for several days. Both Trx-Tg and aged wild-type mice injected with rhTrx were normotensive, showed increased NO production, decreased arterial stiffness, and increased vascular relaxation. These studies suggest that rhTrx could potentially be a therapeutic molecule to reverse age-related hypertension in humans. The reversal of age-related hypertension by restoring proteins that have undergone age-related modification is conceptually novel in the treatment of hypertension. Trx reverses age-related hypertension via maintaining vascular redox homeostasis, regenerating critical vasoregulatory proteins oxidized due to advancing age, and restoring native function of proteins that have undergone age-related modifications with loss-of function. Recent studies demonstrate that Trx is a promising molecule that may ameliorate or reverse age-related hypertension in older adults.
PURPOSE OF REVIEW: Although the roles of oxidant stress and redox perturbations in hypertension have been the subject of several reviews, role of thioredoxin (Trx), a major cellular redox protein in age-related hypertension remains inadequately reviewed. The purpose of this review is to bring readers up-to-date with current understanding of the role of thioredoxin in age-related hypertension. RECENT FINDINGS:Age-related hypertension is a major underlying cause of several cardiovascular disorders, and therefore, intensive management of blood pressure is indicated in most patients with cardiovascular complications. Recent studies have shown that age-related hypertension was reversed and remained lowered for a prolonged period in mice with higher levels of humanTrx (Trx-Tg). Additionally, injection of human recombinant Trx (rhTrx) decreased hypertension in aged wild-type mice that lasted for several days. Both Trx-Tg and aged wild-type mice injected with rhTrx were normotensive, showed increased NO production, decreased arterial stiffness, and increased vascular relaxation. These studies suggest that rhTrx could potentially be a therapeutic molecule to reverse age-related hypertension in humans. The reversal of age-related hypertension by restoring proteins that have undergone age-related modification is conceptually novel in the treatment of hypertension. Trx reverses age-related hypertension via maintaining vascular redox homeostasis, regenerating critical vasoregulatory proteins oxidized due to advancing age, and restoring native function of proteins that have undergone age-related modifications with loss-of function. Recent studies demonstrate that Trx is a promising molecule that may ameliorate or reverse age-related hypertension in older adults.
Authors: T Matoba; H Shimokawa; M Nakashima; Y Hirakawa; Y Mukai; K Hirano; H Kanaide; A Takeshita Journal: J Clin Invest Date: 2000-12 Impact factor: 14.808
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Authors: Katharina Wolf-Maier; Richard S Cooper; José R Banegas; Simona Giampaoli; Hans-Werner Hense; Michel Joffres; Mika Kastarinen; Neil Poulter; Paola Primatesta; Fernando Rodríguez-Artalejo; Birgitta Stegmayr; Michael Thamm; Jaakko Tuomilehto; Diego Vanuzzo; Fenicia Vescio Journal: JAMA Date: 2003-05-14 Impact factor: 56.272