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Optimized new Shengmai powder(优化新生脉散方) inhibits myocardial fibrosis in heart failure by regulating the rat sarcoma/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway

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Journal of Traditional Chinese Medicine 2024年第3期44卷 448-457页

作者： ZHANG Zeyu JIA Zhuangzhuang SONG Yuwei ZHANG Xuan WANG Ci WANG Shuai ZHANG Peipei REN Qiuan WANG Xianliang MAO Jingyuan Department of Cardiovascular the First Teaching Hospital of Tianjin University of Traditional Chinese MedicineNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion

OBJECTIVE: Exploring the effect of Optimized New Shengmai powder(优化新生脉散方, ONSMP) on myocardial fibrosis in heart failure(HF) based on rat sarcoma(RAS)/rapidly accelerated fibrosarcoma(RAF)/mitogen-activated protein kinase kinase(MEK)/extracellular regulated protein kinases(ERK) signaling pathway. METHODS: Randomized 70 Sprague-Dawley rats into sham(n = 10) and operation(n = 60) groups, then established the HF rat by ligating the left anterior descending branch of the coronary artery. We randomly divided the operation group rats into the model, ONSMP [including low(L), medium(M), and high(H) dose], and enalapril groups. After the 4-week drug intervention, echocardiography examines the cardiac function and calculates the ratios of the whole/left heart to the rat's body weight. Finally, we observed the degree of myocardial fibrosis by pathological sections, determined myocardium collagen(COL) Ⅰ and COL Ⅲ content by enzyme-linked immunosorbent assay, detected the m RNA levels of COL Ⅰ, COL Ⅲ, α-smooth muscle actin(α-SMA), and c-Fos proto-oncogene(c-Fos) by universal real-time, and detected the protein expression of p-RAS, p-RAF, p-MEK1/2, p-ERK1/2, p-ETS-like-1 transcription factor(p-ELK1), p-c-Fos, α-SMA, COL Ⅰ, and COL Ⅲ by Western blot. RESULTS: ONSMP can effectively improve HF rat's cardiac function, decrease cardiac organ coefficient, COL volume fraction, and COL Ⅰ/Ⅲ content, down-regulate the m RNA of COL Ⅰ/Ⅲ, α-SMA and c-Fos, and the protein of p-RAS, p-RAF, p-MEK1/2, p-ERK1/2, p-ELK1, c-Fos, COL Ⅰ/Ⅲ, and α-SMA. CONCLUSIONS: ONSMP can effectively reduce myocardial fibrosis in HF rats, and the mechanism may be related to the inhibition of the RAS/RAF/MEK/ERK signaling pathway.

关键词： extracellular regulated protein kinases heart failure mitogen-activated protein kinases myocardial fibrosis optimized new Shengmai powder rapidly accelerated fibrosarcoma sarcoma

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Tongxinluo Activates PI3K/AKT Signaling Pathway to Inhibit Endothelial Mesenchymal Transition and Attenuate myocardial fibrosis after Ischemia-Reperfusion in Mice

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Chinese Journal of Integrative Medicine 2024年第7期30卷 608-615页

作者： WEI Ya-ru HOU Yun-long YIN Yu-jie LI Zhen LIU Yi HAN Ning-xin WANG Zi-xuan LIU Lu WANG Xiao-qi HAO Yuan-jie MA Kun GU Jiao-jiao JIA Zhen-hua Graduate School Hebei University of Chinese Medicine Shijiazhuang Yiling Pharmaceutical New Drug Evaluation Center Hebei Institute of Integrated Traditional and Western Medicine National Key Laboratory for Innovation and Transformation of Luobing Theory Department of Cardiology Hebei Yiling Hospital Graduate School Hebei Medical University

Objective: To investigate the potential role of Tongxinluo(TXL) in attenuating myocardial fibrosis after myocardial ischemia-reperfusion injury(MIRI) in mice. Methods: A MIRI mouse model was established by left anterior descending coronary artery ligation for 45 min. According to a random number table, 66 mice were randomly divided into 6 groups(n=11 per group): the sham group, the model group, the LY-294002 group, the TXL group, the TXL+LY-294002 group and the benazepril(BNPL) group. The day after modeling, TXL and BNPL were administered by gavage. Intraperitoneal injection of LY-294002 was performed twice a week for 4 consecutive weeks. Echocardiography was used to measure cardiac function in mice. Masson staining was used to evaluate the degree of myocardial fibrosis in mice. Qualitative and quantitative analysis of endothelial mesenchymal transition(EndMT) after MIRI was performed by immunohistochemistry, immunofluorescence staining and flow cytometry, respectively. The protein expressions of platelet endothelial cell adhesion molecule-1(CD31), α-smoth muscle actin(α-SMA), phosphatidylinositol-3-kinase(PI3K) and phospho protein kinase B(p-AKT) were assessed using Western blot. Results: TXL improved cardiac function in MIRI mice, reduced the degree of myocardial fibrosis, increased the expression of CD31 and inhibited the expression of α-SMA, thus inhibited the occurrence of EndMT(P0.05). In addition, the use of the PI3K/AKT pathway-specific inhibitor LY-294002 to block this pathway and combination with TXL intervention, eliminated the protective effect of TXL, further supporting the protective effect of TXL. Conclusion: TXL activated the PI3K/AKT signaling pathway to inhibit EndMT and attenuated myocardial fibrosis after MIRI in mice.

关键词： myocardial fibrosis endothelial mesenchymal transition myocardial ischemia-reperfusion injury phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway

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Glycine Attenuates myocardial fibrosis in myocardial Infarction in Rats Partly through Modulating Signal Transducer and Activator of Transcription 3/Nuclear Factor-κB/Transforming Growth Factor-β axis

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World Journal of Traditional Chinese Medicine 2024年第2期10卷 263-270页

作者： Ning Li Yong Wang Chun Li Xu Chen Xue-Feng Zhang Nan-Nan Tan Yi-Qin Hong Ming-Yan Shao Bing-Hua Tang Dong-Qing Guo School of Life Science Beijing University of Chinese Medicine College of Traditional Chinese Medicine Beijing University of Chinese Medicine Modern Research Center of Traditional Chinese Medicine School of Traditional Chinese Material Medica Beijing University of Chinese Medicine

Objective: Inflammation and fibrosis are strongly associated with each other. Glycine is present in various traditional Chinese medicines and exhibits anti-inflammatory activity. However, the effects of glycine on myocardial fibrosis(MF) in rats with myocardial infarction(MI) have not been reported. The purpose of this study is to investigate the effects of glycine therapy on MF and comprehend its underlying mechanisms. Materials and Methods: Left anterior descending artery ligation-induced MI in Sprague Dawley rats was leveraged to assess the therapeutic effects of Glycine. Rats received either normal saline or glycine(0.5 mg/g bodyweight) for 7 days. Results: Glycine upregulated cardiac ejection fraction and fractional shortening to improve cardiac function, as evaluated by echocardiography. Histological and immunohistochemical analyses demonstrated that glycine could decrease inflammatory cell infiltration and alleviate collagen deposition. Western blotting revealed that nuclear factor-κB(NF-κB)-mediated inflammatory signaling was also downregulated by glycine treatment. The expression of signal transducer and activator of transcription 3(STAT3), tumor necrosis factor-α, and transforming growth factor-β(TGF-β) was decreased significantly in the glycine-treated group compared to the model group. Thus, glycine plays a protective role against myocardial ischemia and subsequent MF. Conclusion: The protective effects of glycine were achieved partly through STAT3/NF-κB/TGF-β signaling pathway.

关键词： activator of transcription 3/nuclear factor‑κB/transforming growth factor‑β Glycine myocardial fibrosis signal transducer

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Electroacupuncture improves myocardial fibrosis in heart failure rats by attenuating ECM collagen deposition through modulation of TGF-β1/Smads signaling pathway

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Traditional Medicine Research 2024年第8期9卷 1-10页

作者： Wen-Hui Wang Qian-Lan Zeng Jiao-Jiao Zhang Hao-Sheng Wu Sheng-Bing Wu Mei-Qi Zhou College of Acupuncture and Massage Anhui University of Chinese MedicineHefei 230038China Anhui Province Key Laboratory of Meridian Viscera Correlationship Anhui University of Chinese MedicineHefei 230038China

Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure treatment. Methods: Healthy male Sprague-Dawley rats were allocated into three groups: Sham group, Model group, and electroacupuncture (Model + EA) group, with each group comprising 8 rats. The model underwent a procedure involving the ligation of the left anterior descending coronary artery to induce a model of heart failure. The Model + EA group was used for 7 consecutive days for electroacupuncture of bilateral Shenmen (HT7) and Tongli (HT5), once a day for 30 min each time. Left ventricular parameters in rats were assessed using a small-animal ultrasound machine to analyze changes in left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction, and left ventricular fractional shortening. Serum interleukin-1β (IL-1β), cardiac troponin (cTn), and N-terminal brain natriuretic peptide precursor levels were measured using ELISA. Histopathological changes in rat myocardium were observed through HE staining, while collagen deposition in rat myocardial tissue was assessed using the Masson staining method. Picro sirius red staining, immunohistochemical staining, and RT-qPCR were utilized to distinguish between the various types of collagen deposition. The expression level of TGF-β1 and SMAD2/3/4/7 mRNA in rat myocardial tissues was determined using RT-qPCR. Additionally, western blot analysis was conducted to assess the protein expression levels of TGF-β1, SMAD3/7, and p-SMAD3 in rat myocardial tissues. Results: Compared with the Sham group, the left ventricular ejection fraction and left ventricular fractional shortening values of the Model group were significantly decreased (P < 0.01);the left ventricular end-diastolic volume and left ventricular end-systolic volume values were remarkably increased (P < 0.01);serum N-terminal brain natriuretic peptide prec

关键词： heart failure electroacupuncture heart meridian of Hand-Shaoyin collagen deposition TGF-β1/Smads signaling pathway myocardial fibrosis

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Shenmai Injection Improves Hypertensive Heart Failure by Inhibiting myocardial fibrosis via TGF-β1/Smad Pathway Regulation

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Chinese Journal of Integrative Medicine 2023年第2期29卷 119-126页

作者： HU Si-yuan ZHOU Yao ZHONG Sen-jie YANG Meng HUANG Shu-min LI Lin LI Xin-chun HU Zhi-xi School of Sports Art Hunan University of Chinese MedicineChangsha 410208China College of Health Science Wuhan Sports UniversityWuhan 430079China Department of Medicine Hunan Traditional Chinese Medical CollegeZhuzhouHunan Province 412012China Graduate School Hunan University of Chinese MedicineChangsha 410208China Institute of Chinese Medicine Diagnosis Hunan University of Chinese MedicineChangsha 410208China

Objective: To study effects of Shenmai Injection on hypertensive heart failure and its mechanism for inhibiting myocardial fibrosis. Methods: Salt-sensitive(Dahl/SS) rats were fed with normal diet(0.3% Na Cl) and the high-salt diet(8% Na Cl) to observe the changes in blood pressure and heart function, as the control group and the model group. Salt-insensitive rats(SS-13BN) were fed with the high-salt diet(8% Na Cl) as the negative control group. After modeling, the model rats were randomly divided into heart failure(HF) group, Shenmai Injection(SMI) group and pirfenidone(PFD) group by a random number table, with 6 rats in each group. They were given sterilized water, SMI and pirfenidone, respectively. Blood pressure, cardiac function, fibrosis and related molecular expression were detected by sphygmomanometer, echocardiogram, enzyme linked immunosorbent assay(ELISA),hematoxylin-eosin staining, Masson staining, immunofluorescence and qPCR analysis. Results: After high-salt feeding, compared with the control and negative control group, in the model group the blood pressure increased significantly, the left ventricular ejection fraction(LVEF) and left ventricular fraction shortening(LVFS) were significantly reduced, and the serum NT-pro BNP concentration increased significantly(all Pmyocardial cells was disordered, the edema was severe, and the degree of myocardial fibrosis was also significantly increased(Pmyocardial morphology was improved, collagen volume fraction decreased significantly(Pmyocardial fibrosis i

关键词： myocardial fibrosis heart failure Shenmai Injection transforming growth factorβ1/smad hyperlension

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Involvement of Interleukin-1β/Insulin-Like Growth Factor1in Ameliorating Effects of Electroacupuncture on myocardial fibrosis Induced by Essential Hypertension

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Chinese Journal of Integrative Medicine 2023年第2期29卷 162-169页

作者： XIN Juan-juan GAO Jun-hong LIU Qun ZHAO Yu-xue ZHOU Chen YU Xiao-chun Institute of Acupuncture and Moxibustion China Academy of Chinese Medical SciencesBeijing 100700China

Objective: To investigate the effect of electroacupuncture(EA) at Neiguan(PC 6) on myocardial fibrosis in spontaneously hypertensive rats(SHRs), and to explore the contribution of interleukin-1β(IL-1β),insulin-like growth factor 1(IGF-1), and transforming growth factor β1(TGF-β1) to the effects. Methods:Nine 12-weeks-old Wistar Kyoto(WKY) male rats were employed as the normal group. Twenty-seven SHRs were equally randomized into SHR, SHR+EA, and SHR + sham groups. EA was applied at bilateral PC 6once a day 30 min per day in 8 consecutive weeks. After 8-weeks EA treatment at PC 6, histopathologic changes of collagen type Ⅰ(Col Ⅰ), collagen type Ⅲ(Col Ⅲ) and the levels of IGF-1, 1L-1β, TGF-β1,matrix metalloproteinase(MMP)-2 and MMP-9 were examined in myocardial tissure respectively. Results:After 8-weeks EA treatment at PC 6, the enhanced myocardial fibrosis in SHRs were characterized by the increased mean fluorescence intensity of Col Ⅰ and Col Ⅲ in myocardium tissue(Pmyocardial tissue of SHRs, diminished MMP 9mRNA expression in SHRs were also markedly inhibited after 8 weeks of EA treatment(Pmyocardial tissue were positively correlated with the systolic blood pressure and hydroxyproline respectively(Pfibrosis in SHRs, which might be mediated by regulation of 1L-1β/IGF-1-TGF-β1-MMP9 pathway.

关键词： electroacupuncture spontaneously hypertensive rats myocardial fibrosis interleukin-1β insulin-like growth factor 1

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Liraglutide Suppresses myocardial fibrosis Progression by Inhibiting the Smad Signaling Pathway

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Current Medical Science 2023年第5期43卷 955-960页

作者： Wen SUN Hong MI De-ying HE Wen LI Yi-yan SONGYANG Department of Geriatrics Chongqing Hospital of Traditional Chinese MedicineChongqing 400021China Department of Traditional Chinese Medicine Chongqing Hospital of Traditional Chinese MedicineChongqing 400021China Department of Emergency Renmin Hospital of Wuhan UniversityWuhan 430060China Department of Pharmacy Renmin Hospital of Wuhan UniversityWuhan 430060China

Objective Liraglutide is a commonly used hypoglycemic agent in clinical practice,and has been demonstrated to have protective effects against the development of cardiovascular disease.However,its potential role in myocardial fibrosis remains unexplored.The present study aims to assess the impact of liraglutide on the activation of cardiac fibroblasts.Methods Primary rat adult fibroblasts were isolated,cultured,and randomly allocated into 4 groups:control group,transforming growth factor beta1(TGFβ1)stimulation group,liraglutide group,and TGFβ1+liraglutide group.Fibroblast activation was induced by TGFβ1.Cell proliferation activity was assessed using the CKK-8 kit,and cellular activity was determined using the MTT kit.Reverse transcrition-quantitative polymerase chain reaction(RT-qPCR)was utilized to quantify the level of collagen transcription,immunofluorescence staining was performed to detect the expression level of type III collagen andα-smooth muscle protein(α-SMA),and immunoblotting was conducted to monitor alterations in signal pathways.Results The addition of 10,25,50 and 100 nmol/L of liraglutide did not induce any significant impact on the viability of fibroblasts(P>0.05).The rate of cellular proliferation was significantly higher in the TGFβl stimulation group than in the control group.However,the treatment with 50 and 100 nmol/L of liraglutide resulted in the reduction of TGFβl-induced cell proliferation(P<0.05).The RT-qPCR results revealed that the transcription levels of type I collagen,type III collagen,andα-SMA were significantly upregulated in the TGFβl stimulation group,when compared to the control group(P<0.05).However,the expression levels of these aforementioned factors significantly decreased in the TGFβl+liraglutide group(P<0.05).The immunofluorescence staining results revealed a significant increase in the expression levels of type III collagen andα-SMA in the TGFβl stimulation group,when compared to the control group(P<0.05).However,these expression levels significantly decreased in the TG

关键词： liraglutide myocardial fibrosis TGFβl smad

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Atorvastatin ameliorated myocardial fibrosis in db/db mice by inhibiting oxidative stress and modulating macrophage polarization

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World Journal of Diabetes 2023年第12期14卷 1849-1861页

作者： Xian-Min Song Meng-Nan Zhao Gui-Zhi Li Na Li Ting Wang Hong Zhou Department of Endocrinology The Second Hospital of Hebei Medical UniversityShijiazhuang 050000Hebei ProvinceChina Department of Geriatrics Handan Central HospitalHandan 056001Hebei ProvinceChina

BACKGROUND People with diabetes mellitus(DM)suffer from multiple chronic complications due to sustained hyperglycemia,especially diabetic cardiomyopathy(DCM).Oxidative stress and inflammatory cells play crucial roles in the occurrence and progression of myocardial remodeling.Macrophages polarize to two distinct phenotypes:M1 and M2,and such plasticity in phenotypes provide macrophages various biological functions.AIM To investigate the effect of atorvastatin on cardiac function of DCM in db/db mice and its underlying mechanisms.METHODS DCM mouse models were established and randomly divided into DM,atorvastatin,and metformin groups.C57BL/6 mice were used as the control.Cardiac function was evaluated by echocardiography.Hematoxylin and eosin and Masson staining was used to examine the morphology and collagen fibers in myocardial tissues.The expression of transforming growth factor-β1(TGF-β1),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),M1 macrophages(iNOS^(+)),and M2 macrophages(CD206^(+))were demonstrated by immunohistochemistry and immunofluorescence staining.The levels of TGF-β1,IL-1β,and TNF-αwere detected by ELISA and real-time quantitative polymerase chain reaction.Malondialdehyde(MDA)concentrations and superoxide dismutase(SOD)activities were also measured.RESULTS Treatment with atorvastatin alleviated cardiac dysfunction and decreased db/db mice. The broken myocardialfibers and deposition of collagen in the myocardial interstitium were relieved especially by atorvastatin treatment.Atorvastatin also reduced the levels of serum lactate dehydrogenase, creatine kinase isoenzyme, and troponin;lowered the levels of TGF-β1, TNF-α and IL-1β in serum and myocardium;decreased the concentration of MDAand increased SOD activity in myocardium of db/db mice;inhibited M1 macrophages;and promoted M2macrophages.CONCLUSION Administration of atorvastatin attenuates myocardial fibrosis in db/db mice, which may be associated with theantioxidative stress and anti-inflammatory effects of atorvastatin on diabetic myocardiu

关键词： Atorvastatin Diabetic cardiomyopathy myocardial fibrosis Macrophage polarization Inflammation Oxidative stress

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Association of electrocardiographic markers with myocardial fibrosis as assessed by cardiac magnetic resonance in different clinical settings

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World Journal of Cardiology 2022年第9期14卷 483-495页

作者： George Bazoukis Sebastian Garcia-Zamora GökselÇinier Sharen Lee Enes Elvin Gul JesúsÁlvarez-García Gabi Miana Mertİlker Hayıroğlu Gary Tse Tong Liu Adrian Baranchuk Department of Cardiology Larnaca General HospitalLarnaca 6036Cyprus Department of Basic and Clinical Sciences University of Nicosia Medical SchoolNicosia 2414Cyprus Department of Cardiology Delta ClinicSanta Fe 341Argentina Department of Cardiology Dr.Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research CenterIstanbul 34668Turkey Cardiovascular Analytics Group Laboratory of Cardiovascular PhysiologyHong Kong 999077China Division of Cardiac Electrophysiology Madinah Cardiac CentreMadinah 42351Saudi Arabia Department of Cardiology Ramon y Cajal University HospitalMadrid 28034Spain Telehealth Center of Hospital das Clínicas Hong Kong 999077China Kent and Medway Medical School CanterburyCanterbury CT27FSUnited Kingdom Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease Department of CardiologyTianjin Institute of CardiologySecond Hospital of TianjinTianjin Medical UniversityTianjin 300211China Department of Cardiology The Second Hospital of Tianjin Medical UniversityTianjin 300211China Department of Cardiology Queen's UniversityOntario K7L 3N6Canada

BACKGROUND Cardiac magnetic resonance(CMR)is a unique tool for non-invasive tissue characterization,especially for identifying fibrosis.AIM To present the existing data regarding the association of electrocardiographic(ECG)markers with myocardial fibrosis identified by CMR-late gadolinium enhancement(LGE).METHODS A systematic search was performed for identifying the relevant studies in Medline and Cochrane databases through February 2021.In addition,we conducted a relevant search by Reference Citation Analysis(RCA)(https://***).RESULTS A total of 32 studies were included.In hypertrophic cardiomyopathy(HCM),fragmented QRS(fQRS)is related to the presence and extent of myocardial fibrosis.fQRS and abnormal Q waves are associated with LGE in ischemic cardiomyopathy patients,while fQRS has also been related to fibrosis in myocarditis.Selvester score,abnormal Q waves,and notched QRS have also been associated with LGE.Repolarization abnormalities as reflected by increased Tp-Te,negative Twaves,and higher QT dispersion are related to myocardial fibrosis in HCM patients.In patients with Duchenne muscular dystrophy,a significant correlation between fQRS and the amount of myocardial fibrosis as assessed by LGE-CMR was observed.In atrial fibrillation patients,advanced inter-atrial block is defined as P-wave duration≥120 ms,and biphasic morphology in inferior leads is related to left atrial fibrosis.CONCLUSION myocardial fibrosis,a reliable marker of prognosis in a broad spectrum of cardiovascular diseases,can be easily understood with an easily applicable ECG.However,more data is needed on a specific disease basis to study the association of ECG markers and myocardial fibrosis as depicted by CMR.

关键词： myocardial fibrosis Late gadolinium enhancement Electrocardiogram Cardiac magnetic resonance

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Injectable decellularized extracellular matrix hydrogel loaded with exosomes encapsulating curcumin for prevention of cardiac fibrosis after myocardial infarction

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Journal of Materials Science & Technology 2023年第36期167卷 50-58页

作者： Yuanyuan Wang Jingjing Wang Chunxia Liu Jingjing Li Kunyan Lu Qian Yu Yanxia Zhang Zhenya Shen Department of Cardiovascular Surgery of the First Affiliated Hospital and Institute for Cardiovascular Science Suzhou Medical College of Soochow UniversitySoochow UniversitySuzhou 215007China State and Local Joint Engineering Laboratory for Novel Functional Polymeric Materials College of ChemistryChemical Engineering and Materials ScienceSoochow UniversitySuzhou 215123China

Excessive cardiac fibrosis impairs cardiac repair after myocardial infarction(MI).In this work,an in-jectable composite hydrogel integrating natural biomaterials,exosomes,and bioactive molecules is de-veloped to prevent or alleviate cardiac fibrosis.Curcumin,a natural molecule with antifibrotic activity,is encapsulated in the exosomes that are isolated from bone marrow-derived mesenchymal stem cells to enhance its water solubility and bioavailability.These composite exosomes are efficiently internalised by fibroblasts and effectively inhibit their transition to myofibroblasts in vitro.Decellularized porcine cardiac extracellular matrix(dECM)hydrogel is used as the carrier for delivering these composite exosomes to the infarcted myocardium,not only improving the retention of exosomes but also providing mechani-cal support and structural protection.Injection of this hydrogel into the infarcted heart of a mouse MI model leads to a decrease in collagen deposition,alleviation of fibrosis,a reduction in infarct size,and an improvement in cardiac function.The reported composite hydrogel comprising natural materials and biomolecules exhibits good biocompatibility and bioactivity.Altogether,this study demonstrates that the dECM hydrogel is a suitable platform for the local delivery of antifibrotic biomolecule-encapsulating exo-somes to prevent myocardial fibrosis after MI and have great potential for the treatment of MI in clinical settings.

关键词： myocardial fibrosis myocardial infarction Decellularized extracellular matrix Exosomes Curcumin

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