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Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling.

Abstract

Diabetic cardiomyopathy (DCM), a significant contributor to morbidity and mortality in diabetic patients, is characterized by ventricular dysfunction, in the absence of coronary atherosclerosis and hypertension. There is no specific therapeutic strategy to effectively treat patients with DCM, due to a lack of a mechanistic understanding of the disease process. Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). RAR/RXR-mediated signaling has been implicated in the regulation of glucose and lipid metabolism. Recently, it has been reported that activation of RAR/RXR has an important role in preventing the development of diabetic cardiomyopathy, through improving cardiac insulin resistance, inhibition of intracellular oxidative stress, NF-κB-mediated inflammatory responses and the renin-angiotensin system. Moreover, downregulated RAR/RXR signaling has been demonstrated in diabetic myocardium, suggesting that impaired RAR/RXR signaling may be a trigger to accelerate diabetes-induced development of DCM. Understanding the molecular mechanisms of retinoid receptors in the regulation of cardiac metabolism and remodeling under diabetic conditions is important in providing the impetus for generating novel therapeutic approaches for the prevention and treatment of diabetes-induced cardiac complications and heart failure.

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  • Authors+Show Affiliations

    ,

    Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center, Baylor Scott & White Health, Central Texas Veterans Health Care System, Temple, TX, 76504, USA. jpan@medicine.tamhsc.edu.

    ,

    Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center, Baylor Scott & White Health, Central Texas Veterans Health Care System, Temple, TX, 76504, USA. rsguleria@medicine.tamhsc.edu.

    ,

    Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center, Baylor Scott & White Health, Central Texas Veterans Health Care System, Temple, TX, 76504, USA. szhu@medicine.tamhsc.edu.

    Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A & M Health Science Center, Baylor Scott & White Health, Central Texas Veterans Health Care System, Temple, TX, 76504, USA. kbaker@medicine.tamhsc.edu.

    Source

    Journal of clinical medicine 3:2 2014 Jun 04 pg 566-94

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    26237391

    Citation

    Pan, Jing, et al. "Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling." Journal of Clinical Medicine, vol. 3, no. 2, 2014, pp. 566-94.
    Pan J, Guleria RS, Zhu S, et al. Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling. J Clin Med. 2014;3(2):566-94.
    Pan, J., Guleria, R. S., Zhu, S., & Baker, K. M. (2014). Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling. Journal of Clinical Medicine, 3(2), pp. 566-94. doi:10.3390/jcm3020566.
    Pan J, et al. Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling. J Clin Med. 2014 Jun 4;3(2):566-94. PubMed PMID: 26237391.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Molecular Mechanisms of Retinoid Receptors in Diabetes-Induced Cardiac Remodeling. AU - Pan,Jing, AU - Guleria,Rakeshwar S, AU - Zhu,Sen, AU - Baker,Kenneth M, Y1 - 2014/06/04/ PY - 2014/02/19/received PY - 2014/03/17/revised PY - 2014/03/25/accepted PY - 2015/8/4/entrez PY - 2014/1/1/pubmed PY - 2014/1/1/medline KW - diabetes mellitus KW - diabetic cardiomyopathy KW - retinoic acid KW - retinoic acid receptor KW - retinoid X receptor SP - 566 EP - 94 JF - Journal of clinical medicine JO - J Clin Med VL - 3 IS - 2 N2 - Diabetic cardiomyopathy (DCM), a significant contributor to morbidity and mortality in diabetic patients, is characterized by ventricular dysfunction, in the absence of coronary atherosclerosis and hypertension. There is no specific therapeutic strategy to effectively treat patients with DCM, due to a lack of a mechanistic understanding of the disease process. Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). RAR/RXR-mediated signaling has been implicated in the regulation of glucose and lipid metabolism. Recently, it has been reported that activation of RAR/RXR has an important role in preventing the development of diabetic cardiomyopathy, through improving cardiac insulin resistance, inhibition of intracellular oxidative stress, NF-κB-mediated inflammatory responses and the renin-angiotensin system. Moreover, downregulated RAR/RXR signaling has been demonstrated in diabetic myocardium, suggesting that impaired RAR/RXR signaling may be a trigger to accelerate diabetes-induced development of DCM. Understanding the molecular mechanisms of retinoid receptors in the regulation of cardiac metabolism and remodeling under diabetic conditions is important in providing the impetus for generating novel therapeutic approaches for the prevention and treatment of diabetes-induced cardiac complications and heart failure. SN - 2077-0383 UR - https://www.unboundmedicine.com/medline/citation/26237391/Molecular_Mechanisms_of_Retinoid_Receptors_in_Diabetes_Induced_Cardiac_Remodeling_ L2 - http://www.mdpi.com/resolver?pii=jcm3020566 DB - PRIME DP - Unbound Medicine ER -