Role of puerarin in pathological cardiac remodeling: A review. (April 2022)

• Record Type: Journal Article
• Authors: Lv, Jiayu; Shi, Shuqing; Zhang, Bingxuan; Xu, Xia; Zheng, Haoran; Li, Yumeng; Cui, Xiangning; Wu, Huaqin; Song, Qingqiao
• Is Part Of: Pharmacological research. Volume 178(2022)
• Publication Date: 2022-04
• Subjects: Puerarin (PubChem CID:5281807); MI myocardial infarction -- HF heart failure -- FGFs fibroblast growth factors -- ACEI angiotensin-converting enzyme inhibitors -- ARB angiotensin II receptor blockers -- NPs natural products -- TCM Traditional Chinese medicine -- ECM extracellular matrix -- RAAS renin-angiotensin-aldosterone system -- ET-1 endothelin-1 -- EndMT endothelial mesenchymal transition -- MMP matrix metalloproteinase -- DAMPs danger-associated molecular patterns -- GPCRs G protein-coupled receptors -- OMM outer mitochondrial membrane -- MOMP mitochondrial outer membrane permeabilization -- IMM inner mitochondrial membrane -- ARE antioxidant response element -- mtROS ROS produced in the mitochondria -- AMI acute myocardial infarction -- 4EBP1 4E-binding protein 1 -- AAC abdominal aortic constriction -- A/R anoxia/reoxygenatio -- AB aortic banding -- Akt protein kinase B -- Ang II angiotensin Ⅱ -- Ang-1 angiopoietin-1 -- Ang-2 angiopoietin-2 -- ANP atrial natriuretic peptide -- ANRIL antisense non-coding RNA in the INK4 locus -- AP-1 activating protein-1 -- Bax Bcl-2 associated X protein -- Bcl-2 B-cell lymphoma-2 -- CAT catalase；CD36, cluster of differentiation 36 -- CK-MB creatine kinase MB -- CPK creatine kinase isoenzymes -- CTGF connective tissue growth factor -- CVF collagen volume fraction -- CWI cardiac weight index -- DBP diastolic blood pressure -- dP/dt max maximal rise/fall rate of left ventricular pressure -- EDP end-diastolic pressure -- EndMT endothelial-to-mesenchymal transition -- eNOS endothelial nitric oxide synthase -- ERK1/2 extracellular regulated protein kinases 1/2 -- FATP1 fatty acid transport protein 1 -- FFA free fatty acid -- FoxO1 forkhead box O1 -- FoxO3a forkhead box O3a -- FSP1 fibroblast protein-1 -- GLUT4 glucose transporter 4 -- GSH-Px glutathione peroxidase -- GSK3β glycogen synthase kinase 3β -- GSTP1 glutathione-S-transferase P1 -- H/R hypoxia/reoxygenation -- HCAECs human coronary artery endothelial cells -- HFD high-fat diet -- HMGB1 high mobility group protein B1 -- HO1 heme oxygenase 1 -- HUVECs human umbilical vein endothelial cells -- HW/BW heart weight/body weight -- HW/TL heart weight/tibial length -- HYP hydroxyproline -- IL-1β interleukin-1β -- IL-6 interleukin-6 -- IL-8 interleukin-8 -- ISO isoprenaline -- IVSd interventricular end-diastolic septum thickness -- IVSs interventricular septum endsystolic thickness -- IVSth interventricular septal wall thickness -- JNK1/2 c-Jun amino-terminal kinase 1/2 -- Keap 1 Kelch-Like ECH-Associated Protein 1 -- K-H Krebs-Henseleit -- LAD left anterior descending -- LC3 light chain 3 -- LC3B-II light chain B-II -- LDH layered double hydroxide -- LPS lipopolysaccharide -- LVEDD left ventricular end-diastolic diameter -- LVEDP left ventricular end-diastolic pressure -- LVEF left ventricular ejection fraction -- LVESD left ventricular end-systolic diameter -- LVESP left ventricular end-systolic pressure -- LVFS left ventricular fractional shortening -- LVId left ventricular interior diameter -- LVIDd left ventricle internal diameters -- LVIDs left ventricular internal dimension systole -- LVPWd left ventricular posterior wall dimension -- LVPWs left ventricular posterior wall end-systolic thickness -- LVPWth left ventricular posterior wall thickness -- LVW/BW left ventricular weight to body weight -- LW/BW lung weight/body weight -- MAPK AMP-activated protein kinase -- MCP-1 monocyte chemoattractant protein-1 -- MCSA myocyte cross sectional area -- MDA malondialdehyde -- mitoKATP mitochondrial ATP-sensitive potassium -- mitoKCa mitochondrial calcium-activated potassium -- MMP-2 matrix metalloproteinases-2 -- MMP-9 matrix metalloproteinases-9 -- mPTP mitochondrial permeability transition pore -- mTOR mammalian target of rapamycin -- Myh7 beta myosin heavy chain -- NADPH nicotinamide adenine dinucleotide phosphate -- NF-κB nuclear factor kappa-B -- NLRP3 nod-like receptor family pyrin domain containing 3 -- NO nitric oxide -- NOX2 NADPH oxidase 2；NQO1, quinone oxidoreductase 1 -- NRCFs Neonatal Rat Cardiac Fibroblasts -- NRCMs neonatal rat cardiomyocytes -- NRCs Neonatal rat cardiomyocytes -- Nrf2 nuclear factor erythroid 2-related factor 2 -- PI3K phosphatidylinositol 3-kinase -- PKCε protein kinase C ε -- PPAR-γ proliferator-activated receptor-γ -- ROS reactive oxygen species -- RPP rate-pressure product (RPP: LVDP * HR) -- S6K p70S6 Kinase -- SBP systolic blood pressure -- SERCA2α sarcoplasmatic reticulum calcium ATPase 2 Alpha -- SIRT1 silent information regulator 1 -- SOD superoxide dismutase -- STZ-NA Streptozotocin-Nicotinamide -- TAC transverse aorta constriction -- TGF-β1 transforming growth factor β 1 -- TLR4 Toll-like receptor 4 -- TNF-α tumor necrosis factor-α -- UGT1A1 uridine diphosphate -glucuronosyltransferase 1A1 -- UGT1A9 uridine diphosphate -glucuronosyltransferase 1A9 -- VEGF vascular endothelial growth factor -- VEGFA vascular endothelial growth factor A -- α-MHC α -myosin heavy polypeptide -- α-SMA alpha smooth muscle actin -- β -MHC β -myosin heavy polypeptide -- Δψm mitochondrial membrane potential -- vWF Agvon Willebrand factor -- LPO lipid peroxidation -- TXB2 thromboxane B2 -- 6 K-PGF1α 6-keto-prostaglandin F1 alpha; Puerarin -- Traditional Chinese medicine -- Pathological cardiac remodeling -- Pharmacological effect; Pharmacology -- Periodicals; Pharmacology -- Periodicals; Research -- Periodicals; Médicaments -- Recherche -- Périodiques; Pharmacologie -- Périodiques; 615.105
• DOI: 10.1016/j.phrs.2022.106152
• Languages: English
• ISSNs: 1043-6618

Abstract

Abstract: Pathological cardiac remodeling normally involves changes in structure, function, and energy metabolism of the heart induced by cardiac injury or load, terminally leading to heart failure. Cardiac remodeling plays an essential role in the progression of cardiovascular disease, thus increasingly identified as an important therapeutic target for heart failure of all pathogenesis. Puerarin, as a natural isoflavone mainly from Pueraria lobata （Willd.）Ohwi, has been developed as injections, eye drops, microemulsions, etc., and is widely used in the clinical treatment of cardiovascular diseases in eastern Asia countries. In recent years, a growing number of studies have shown that puerarin significantly inhibits myocardial hypertrophic growth, myocyte death, fetal gene expression, fibroblast proliferation and activation, improves energy metabolism, promotes post-infarction angiogenesis, and suppresses inflammation and oxidative stress, consequently attenuating or preventing cardiac remodeling in response to multiple stimuli ( e.g., pressure overload, MIRI, MI, Iso, and Ang II stimulation). This review summarized the roles and underlying molecular mechanisms of puerarin in cardiac remodeling induced by diverse etiologies, aiming to help develop novel therapeutic strategies to prevent or reverse pathological ventricular remodeling. Graphical Abstract: ga1