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Review
. 2017:2017:8214541.
doi: 10.1155/2017/8214541. Epub 2017 Oct 24.

Roles and Mechanisms of Herbal Medicine for Diabetic Cardiomyopathy: Current Status and Perspective

Affiliations
Review

Roles and Mechanisms of Herbal Medicine for Diabetic Cardiomyopathy: Current Status and Perspective

Jinfan Tian et al. Oxid Med Cell Longev. 2017.

Abstract

Diabetic cardiomyopathy is one of the major complications among patients with diabetes mellitus. Diabetic cardiomyopathy (DCM) is featured by left ventricular hypertrophy, myocardial fibrosis, and damaged left ventricular systolic and diastolic functions. The pathophysiological mechanisms include metabolic-altered substrate metabolism, dysfunction of microvascular, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, cardiomyocyte apoptosis, mitochondrial dysfunction, and impaired Ca2+ handling. An array of molecules and signaling pathways such as p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), and extracellular-regulated protein kinases (ERK) take roles in the pathogenesis of DCM. Currently, there was no remarkable effect in the treatment of DCM with application of single Western medicine. The myocardial protection actions of herbs have been gearing much attention. We present a review of the progress research of herbal medicine as a potential therapy for diabetic cardiomyopathy and the underlying mechanisms.

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Figures

Figure 1
Figure 1
Pathophysiological mechanisms for DCM. RASS: renin-angiotensin-aldosterone system; DCM: diabetic cardiomyopathy.
Figure 2
Figure 2
Inflammation cascade in pathogenesis of DCM. AMPK: AMP activated-protein kinase; MAPK: mitogen-activated protein kinase; SIRT1: sirtuin 1; IKK: IκB kinase; RE: response element; PPAR: peroxisome proliferator-activated receptor; PGC1α: PPAR-γ co-activator-1; RXR: retinoid X receptor; PPRE: PPAR response elements; TNF-α: tumor necrosis factor-α; IL: interleukin.
Figure 3
Figure 3
Potential Mechanisms of herbal medicine protects against diabetic cardiomyopathy. Nrf2: transcription factor NFE2-related factor 2.
Figure 4
Figure 4
Metabolic regulation for normal heart. LCFA: long-chain fatty acids; FAT/CD36: translocation of FA transporter; GLUT: glucose transporter proteins; ACC: acetyl-COA carboxylase; ACS: acyl-CoA synthetase; CPT1: carnitine palmitoyltransferase-1; PI3K: phosphatidylinositol 3-kinase; IRS-1: insulin receptor substrate 1.
Figure 5
Figure 5
Molecular structure of the compounds described in this review.

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