Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs

doi:10.19586/j.2095-2341.2026.0008

Current Biotechnology ›› 2026, Vol. 16 ›› Issue (2): 348-355.DOI: 10.19586/j.2095-2341.2026.0008

• Reviews • Previous Articles

Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs

Yan CHEN(), Zhida LIU

School of Pharmacy，Harbin University of Commerce，Harbin 150076，China

Received:2026-01-14 Accepted:2026-02-27 Online:2026-03-25 Published:2026-04-27

Abstract

Abstract:

With the continuous innovation and development of anti-tumor treatment methods， the prognosis of cancer patients has been significantly improved. However， the problem of cardiotoxicity induced by chemotherapeutic drugs has become increasingly prominent. This toxic reaction not only severely limits the choice of treatment regimens for cancer patients but also exerts an important impact on their quality of life and long-term prognosis. This article systematically summarized the clinical manifestations and action mechanisms of cardiotoxicity associated with common chemotherapeutic drugs， reviewed the research progress in prevention and treatment at home and abroad， and sorted out the existing common and new prevention and treatment strategies， in order to provide theoretical reference and practical basis for the clinical management of chemotherapy-induced cardiotoxicity.

Key words: chemotherapy drugs, cardiotoxicity, pathogenesis, novel strategy

CLC Number:

Q819

Yan CHEN, Zhida LIU. Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs[J]. Current Biotechnology, 2026, 16(2): 348-355.

Figures/Tables 1

References 72

[1]	张天竺,吴东凯,罗斌斌,等.抗肿瘤药物的心血管毒性与非临床评价[C]//第四届(2023年)中国安全药理学学术年会论文集.2023:138.
[2]	HERRMANN J. Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia[J]. Nat. Rev. Cardiol., 2020, 17(8): 474-502.
[3]	张冰,萨日娜,张晓朦,等.药源性心脏毒性研究进展[J].中国药物警戒,2023,20(8):841-847.
	ZHANG B, SA R N, ZHANG X M, et al.. Research progress in pharmacogenic cardiotoxicity[J]. Chin. J. Pharmacovigil., 2023, 20(8): 841-847.
[4]	GAO F, XU T, ZANG F, et al.. Cardiotoxicity of anticancer drugs: molecular mechanisms, clinical management and innovative treatment[J]. Drug Des. Devel. Ther., 2024, 18: 4089-4116.
[5]	苏毅馨,朱世杰,高业博,等.化疗相关心脏毒性问题研究进展[J].现代肿瘤医学,2022,30(17):3253-3256.
	SU Y X, ZHU S J, GAO Y B, et al.. Advances on chemotherapy-related cardiotoxicity[J]. J. Mod. Oncol., 2022, 30(17): 3253-3256.
[6]	CAI K, JIANG H, ZOU Y, et al.. Programmed death of cardiomyocytes in cardiovascular disease and new therapeutic approaches[J/OL]. Pharmacol. Res., 2024, 206: 107281[2025-12-01]. .
[7]	李薇,徐晓红.蒽环类药物引发心脏毒性的研究进展[J].中南药学,2024,22(2):437-444.
	LI W, XU X H. Research advance in cardiotoxicity induced by anthracyclines[J]. Cent. South Pharm., 2024, 22(2): 437-444.
[8]	PANTAZI D, TSELEPIS A D. Cardiovascular toxic effects of antitumor agents: pathogenetic mechanisms[J/OL]. Thromb. Res., 2022, 213(): 95-102.
[9]	SEARA F A C, KASAI-BRUNSWICK T H, NASCIMENTO J H M, et al.. Anthracycline-induced cardiotoxicity and cell senescence: new therapeutic option?[J/OL]. Cell. Mol. Life Sci., 2022, 79(11): 568[2025-12-01]. .
[10]	TSCHESCHNER H, MEINHARDT E, SCHLEGEL P, et al.. CaMKII activation participates in doxorubicin cardiotoxicity and is attenuated by moderate GRP78 overexpression[J/OL]. PLoS One, 2019, 14(4): e0215992[2025-12-01]. .
[11]	ALVES M T, CONCEIÇÃO I M C ADA, DE OLIVEIRA A N, et al.. microRNA miR-133a as a biomarker for doxorubicin-induced cardiotoxicity in women with breast cancer: a signaling pathway investigation[J]. Cardiovasc. Toxicol., 2022, 22(7): 655-662.
[12]	BARACHINI S, GHELARDONI S, VARGA Z V, et al.. Antineoplastic drugs inducing cardiac and vascular toxicity-An update[J/OL]. Vasc. Pharmacol., 2023, 153: 107223[2025-12-01]. .
[13]	GAMBARDELLA J, TRIMARCO B, IACCARINO G, et al.. Cardiac nonmyocyte cell functions and crosstalks in response to cardiotoxic drugs[J/OL]. Oxid. Med. Cell. Longev., 2017, 2017: 1089359[2025-12-01]. .
[14]	GOTTDIENER J S. Cardiotoxicity associated with high-dose cyclophosphamide therapy[J/OL]. Arch. Intern. Med., 1981, 141(6): 758[2025-12-01]. .
[15]	IQUBAL A, IQUBAL M K, SHARMA S, et al.. Molecular mechanism involved in cyclophosphamide-induced cardiotoxicity: old drug with a new vision[J]. Life Sci., 2019, 218: 112-131.
[16]	MA W, WEI S, ZHANG B, et al.. Molecular mechanisms of cardiomyocyte death in drug-induced cardiotoxicity[J/OL]. Front. Cell Dev. Biol., 2020, 8: 434[2025-12-01]. .
[17]	ZHAO L. Protective effects of trimetazidine and coenzyme Q10 on cisplatin-induced cardiotoxicity by alleviating oxidative stress and mitochondrial dysfunction[J]. Anatol. J. Cardiol., 2019, 22(5): 232-239.
[18]	JOSHI A M, PROUSI G S, BIANCO C, et al.. Microtubule inhibitors and cardiotoxicity[J/OL]. Curr. Oncol. Rep., 2021, 23(3): 30[2025-12-01]. .
[19]	高阳.培美曲塞和紫杉醇分别联合奈达铂对晚期非小细胞肺癌患者心脏毒性的研究[D].长春:吉林大学,2023.
[20]	LYON A R, LÓPEZ-FERNÁNDEZ T, COUCH L S, et al.. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)[J]. Eur. Heart J., 2022, 43(41): 4229-4361.
[21]	LI D, SONG C, ZHANG J, et al.. ROS and iron homeostasis dependent ferroptosis play a vital role in 5-fluorouracil induced cardiotoxicity in vitro and in vivo [J/OL]. Toxicology, 2022, 468: 153113[2025-12-01]. .
[22]	ABDELMASEIH R, BLANCO A, ABDELMASIH R, et al.. Cardio-oncology: capecitabine can sometimes be heatbreaking capecitabine-induced takotsubo cardiomyopathy case report and literature review[J/OL]. Curr. Probl. Cardiol., 2021, 46(8): 100854[2025-12-01]. .
[23]	REDWANZ C, PIRES R H, BIEDENWEG D, et al.. Endothelin-1 influences mechanical properties and contractility of hiPSC derived cardiomyocytes resulting in diastolic dysfunction[J]. J. Mol. Cell. Cardiol., 2024, 194: 105-117.
[24]	YANG Y, ZHOU Q, GAO A, et al.. Endoplasmic reticulum stress and focused drug discovery in cardiovascular disease[J]. Clin. Chim. Acta, 2020, 504: 125-137.
[25]	KOLIJN D, PABEL S, TIAN Y, et al.. Empagliflozin improves endothelial and cardiomyocyte function in human heart failure with preserved ejection fraction via reduced pro-inflammatory-oxidative pathways and protein kinase Gα oxidation[J]. Cardiovasc. Res., 2021, 117(2): 495-507.
[26]	RAPA S F, MAGLIOCCA G, PEPE G, et al.. Protective effect of pomegranate on oxidative stress and inflammatory response induced by 5-fluorouracil in human keratinocytes[J/OL]. Antioxidants, 2021, 10(2): 203[2025-12-01]. .
[27]	LI W, CHENG X, ZHU G, et al.. A review of chemotherapeutic drugs-induced arrhythmia and potential intervention with traditional Chinese medicines[J/OL]. Front. Pharmacol., 2024, 15: 1340855[2025-12-01]. .
[28]	BATTY M, BENNETT M R, YU E. The role of oxidative stress in atherosclerosis[J/OL]. Cells, 2022, 11(23): 3843[2025-12-01]. .
[29]	ABDUL-RAHMAN T, DUNHAM A, HUANG H, et al.. Chemotherapy induced cardiotoxicity: a state of the art review on general mechanisms, prevention, treatment and recent advances in novel therapeutics[J/OL]. Curr. Probl. Cardiol., 2023, 48(4): 101591[2025-12-01]. .
[30]	LI W, JIANG L H, MA L J, et al.. Research progress of ferroptosis in cardiomyopathy[J]. J. Kunming. Med. Univ., 2024, 45(3): 1-8.
[31]	HUANG Y H, ZHANG G P, LIANG H, et al.. Inhibition of ferroptosis can reduce myocardial injury in sepsis mice:the role of lipocalin-2[J]. J. South. Med. Univ., 2022, 42(2): 256-261.
[32]	LAZZERINI P E, CAPECCHI P L, LAGHI-PASINI F. Long QT syndrome: an emerging role for inflammation and immunity[J/OL]. Front. Cardiovasc. Med., 2015, 2: 26[2025-12-01]..
[33]	TAM A B, MERCADO E L, HOFFMANN A, et al.. ER stress activates NF-κB by integrating functions of basal IKK activity, IRE1 and PERK[J/OL]. PLoS One, 2012, 7(10): e45078[2025-12-01]. .
[34]	RAHMAN I. Oxidative stress, transcription factors and chromatin remodelling in lung inflammation[J]. Biochem. Pharmacol., 2002, 64(5-6): 935-942.
[35]	EL-AZIZ T A, MOHAMED R H, PASHA H F, et al.. Catechin protects against oxidative stress and inflammatory-mediated cardiotoxicity in adriamycin-treated rats[J]. Clin. Exp. Med., 2012, 12(4): 233-240.
[36]	AROMOLARAN A S, SRIVASTAVA U, ALÍ A, et al.. Interleukin-6 inhibition of hERG underlies risk for acquired long QT in cardiac and systemic inflammation[J/OL]. PLoS One, 2018, 13(12): e0208321[2025-12-01]. .
[37]	LI Q, QIN M, TAN Q, et al.. microRNA-129-1-3p protects cardiomyocytes from pirarubicin-induced apoptosis by down-regulating the GRIN2D-mediated Ca²⁺ signalling pathway[J]. J. Cell. Mol. Med., 2020, 24(3): 2260-2271.
[38]	AWAD H H, EL-DERANY M O, MANTAWY E M, et al.. Comparative study on beneficial effects of vitamins B and D in attenuating doxorubicin induced cardiotoxicity in rats: emphasis on calcium homeostasis[J/OL]. Biomed. Pharmacother., 2021, 140: 111679[2025-12-01]. .
[39]	MAMOSHINA P, RODRIGUEZ B, BUENO-OROVIO A. Toward a broader view of mechanisms of drug cardiotoxicity[J/OL]. Cell Rep. Med., 2021, 2(3): 100216[2025-12-01]. .
[40]	TAIMEH Z, LOUGHRAN J, BIRKS E J, et al.. Vascular endothelial growth factor in heart failure[J]. Nat. Rev. Cardiol., 2013, 10(9): 519-530.
[41]	BOUTIN G, YUZUGULEN J, PRANJOL M Z I. Endothelin-based markers for endothelial dysfunction in chemotherapy-induced cardiotoxicity[J/OL]. J. Mol. Cell. Cardiol. Plus, 2023, 6: 100053[2025-12-01]. .
[42]	PONDÉ N F, LAMBERTINI M, DE AZAMBUJA E. Twenty years of anti-HER2 therapy-associated cardiotoxicity[J/OL]. ESMO Open, 2016, 1(4): e000073[2025-12-01]. .
[43]	TANG X X, DAN L. Research progress on mitochondrial energy metabolism in heart failure[J]. Adv. Clin. Med.,2024, 14: 1908-1918.
[44]	JIN N, JIE J. Cardiac aging and mitochondrial therapy[J]. Chin. J. Biochem. Mol. Biol., 2024, 40(5): 1-12.
[45]	GOODWILL A G, DICK G M, KIEL A M, et al.. Regulation of coronary blood flow[J]. Compr. Physiol., 2017, 7(2): 321-382.
[46]	刘昊, 李响. 冠状动脉疾病发病机制及治疗策略研究进展[J]. 生物技术进展, 2025,15(2): 254-262.
	LIU H, LI X.Research progress on the pathogenesis and treatment strategy of coronary artery disease[J]. Prog. Biotechnol., 2025, 15(2): 254-262.
[47]	VOLKOVA M, RUSSELL R 3rd. Anthracycline cardiotoxicity: prevalence, pathogenesis and treatment[J]. Curr. Cardiol. Rev., 2011, 7(4): 214-220.
[48]	JOSEPH P, SWEDBERG K, LEONG D P, et al.. The evolution of β-blockers in coronary artery disease and heart failure (part 1/5)[J]. J. Am. Coll. Cardiol., 2019, 74(5): 672-682.
[49]	PITUSKIN E, MACKEY J R, KOSHMAN S, et al.. Multidisciplinary approach to novel therapies in cardio-oncology research (MANTICORE 101-breast): a randomized trial for the prevention of trastuzumab-associated cardiotoxicity[J]. J. Clin. Oncol., 2017, 35(8): 870-877.
[50]	王媚,张楠,徐柳月,等.β受体阻滞剂对蒽环类药物所致亚临床心脏毒性疗效的meta分析[J].现代医药卫生,2021,37(17):2937-2942.
	WANG M, ZHANG N, XU L Y, et al.. Efficacy of β receptor blockers on subclinical cardiotoxicity induced by anthracyclines: a meta-analysis[J]. J. Mod. Med. Health, 2021, 37(17): 2937-2942.
[51]	BERLINER D, BAUERSACHS J. Current drug therapy in chronic heart failure: the new guidelines of the European society of cardiology (ESC)[J]. Korean Circ. J., 2017, 47(5): 543-554.
[52]	QUAGLIARIELLO V, DE LAURENTIIS M, REA D, et al.. The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin[J/OL]. Cardiovasc. Diabetol., 2021, 20(1): 150[2025-12-01]. .
[53]	MEDINA-HERNÁNDEZ D, CÁDIZ L, MASTRANGELO A, et al.. SGLT2i therapy prevents anthracycline-induced cardiotoxicity in a large animal model by preserving myocardial energetics[J]. JACC Cardio Oncol., 2025, 7(2): 171-184.
[54]	SOBCZUK P, CZERWIŃSKA M, KLEIBERT M, et al.. Anthracycline-induced cardiotoxicity and renin-angiotensin-aldosterone system-from molecular mechanisms to therapeutic applications[J]. Heart Fail. Rev., 2022, 27(1): 295-319.
[55]	ZHANG Y, LIU J, LI Y, et al.. Protective role of enalapril in anthracycline-induced cardiotoxicity: a systematic review[J/OL]. Front. Pharmacol., 2020, 11: 788[2025-12-01]. .
[56]	KATOGIANNIS K, IKONOMIDIS I, FARMAKIS D, et al.. Effect of sacubitril/valsartan or enalapril on left ventricular function in patients with hematologic malignancies treated with bone marrow transplantation: a randomized controlled trial[J/OL]. JACC Adv., 2025, 4(3): 101628[2025-12-01]. .
[57]	郑俊腾.卡维地洛和依那普利对蒽环类药物引起心脏毒性的治疗[D].汕头:汕头大学,2021.
[58]	JIN Z, ZHANG J, ZHI H, et al.. The beneficial effects of tadalafil on left ventricular dysfunction in doxorubicin-induced cardiomyopathy[J]. J. Cardiol., 2013, 62(2): 110-116.
[59]	俞佳慧,巩倩,庄乐南.肺动脉高压动物模型及其在药物研究中的应用进展[J].实验动物与比较医学,2023,43(4):381-397.
	YU J H, GONG Q, ZHUANG L N. Animal models of pulmonary arterial hypertension and their application in drug research[J]. Lab. Anim. Comp. Med., 2023, 43(4): 381-397.
[60]	MA Y, YUAN Q, AIZEZE A, et al.. Statins to prevent anthracyclines-induced cardiotoxicity[J/OL]. Austin Cardiol., 2023, 8(1):1037[2025-12-01]. .
[61]	ABDEL-QADIR H, BOBROWSKI D, ZHOU L, et al.. Statin exposure and risk of heart failure after anthracycline- or trastuzumab-based chemotherapy for early breast cancer: a propensity score-matched cohort study[J/OL]. J. Am. Heart Assoc., 2021, 10(2): e018393[2025-12-01]. .
[62]	SOLIMAN Y, MOUFFOKES A, AMER B E, et al.. Abstract 15440: efficacy of statins in counteracting anthracyclines and/or trastazumab-induced cardiotoxicity: a systematic review and meta-analysis with trial sequential analysis[J/OL]. Circulation, 2023, 148(S1): 1065510[2025-12-01]. .
[63]	JAHNG J W S, LIU L, WU J C. Tumor repressor circular RNA as a new target for preventative gene therapy against doxorubicin-induced cardiotoxicity[J]. Circ. Res., 2020, 127(4): 483-485.
[64]	XIONG W, LI B, PAN J, et al.. Mitochondrial amount determines doxorubicin-induced cardiotoxicity in cardiomyocytes[J/OL].Adv. Sci. 2025, 12(12): e2412017[2025-12-01]. .
[65]	HUO M, TANG Z, WANG L, et al.. Magnesium hexacyanoferrate nanocatalysts attenuate chemodrug-induced cardiotoxicity through an anti-apoptosis mechanism driven by modulation of ferrous iron[J/OL]. Nat. Commun., 2022, 13(1): 7778[2025-12-01]. .
[66]	HUANG J, YANG J, YANG Y, et al.. Mitigating doxorubicin-induced cardiotoxicity and enhancing anti-tumor efficacy with a metformin-integrated self-assembled nanomedicine[J/OL]. Adv. Sci., 2025, 12(17): 2415227[2025-12-01]. .
[67]	胡光文.不同剂量阿霉素化疗对乳腺癌患者引起心脏不良反应的分析[D].扬州:扬州大学,2023.
[68]	姜金龙,计成阜,何广胜,等.生脉注射液结合持续静脉缓慢滴注蒽环类药物降低早期心脏毒性发生风险的临床观察[J]. 现代肿瘤医学,2021,29 (3):499-502.
	JIANG J L, JI C F, HE G S, et al.. Clinical observation of continuous intravenous slow infusion of anthracyclines to reduce the risk of early cardiotoxicity[J]. J. Mod. Oncol., 2021, 29 (3):499-502.
[69]	TANG L, HE M, WU J, et al.. Cardiac safety and efficacy for patients with early-stage breast cancer treated with pegylated liposomal doxorubicin (PLD) or doxorubicin[J/OL]. J. Clin. Oncol., 2023, 41(16): 550[2025-12-01]. .
[70]	李红梅,龚丽景,王勇,等.有氧运动缓解化疗期间乳腺癌患者心脏毒性的效果[J].北京体育大学学报,2023,46(11):143-156.
	LI H M, GONG L J, WANG Y, et al.. Effect of aerobic exercise on alleviating cardiotoxicity of breast cancer patients during chemotherapy[J]. J. Beijing Sport Univ., 2023, 46(11): 143-156.
[71]	DELGADO-LISTA J, ALCALA-DIAZ J F, TORRES-PEÑA J D, et al.. Long-term secondary prevention of cardiovascular disease with a Mediterranean diet and a low-fat diet (CORDIOPREV): a randomised controlled trial[J]. Lancet, 2022, 399(10338): 1876-1885.
[72]	CASINI C, MONZANI D, MASIERO M, et al.. 1432P incorporating psycho-social factors in cancer treatment adverse events studies[J/OL]. Ann. Oncol., 2022, 33: S1199[2025-12-01]. .

常见化疗药物类型	化疗药物名称	心脏毒性作用	分子机制
蒽环类药物	阿霉素、柔红霉素、表柔比星和伊达比星等	心肌细胞死亡；左心室功能障碍，最终降低心排血量^[7]	活性氧（reactive oxygen species，ROS）的生成与自身抗氧化作用的失衡^[8]；由拓扑异构酶Ⅱ与肿瘤结合引起的DNA双链裂解^[9]；细胞内钙超载^[10]； miRNA表达的上调损害心肌细胞线粒体^[11]；促进释放炎症因子^[12]；转化生长因子β信号的增强和肌成纤维细胞的激活^[13]
烷基化试剂	环磷酰胺	程序性细胞凋亡，导致心脏应激和心力衰竭^[14]	环磷酰胺在肝脏分解后产生的丙烯酰胺损害心肌细胞和内皮细胞；降低抗氧化剂的水平，导致心肌细胞中脂肪酸氧化的下调^[15]
铂类药物	顺铂	导致心肌细胞和血管内皮细胞受损，进而引起心肌细胞收缩功能障碍^[16]	扰乱细胞内氧化应激和抗氧化应激的平衡，导致氧自由基增加、DNA损伤和细胞凋亡^[17]
紫杉烷类	紫杉醇、多西他赛	轻度心肌损伤，表现为QT间期延长，心动过缓及心房心室纤维性颤动^[18]	促进微管蛋白聚合并抑制解聚，从而抑制肿瘤细胞形成纺锤体，进一步抑制有丝分裂进程，导致细胞周期停滞，抑制细胞增殖^[19]
代谢拮抗物	5-氟尿嘧啶、卡培他滨、替吉奥、TAS-102等	大部分可逆，导致冠状动脉血管痉挛和血管收缩^[20]	NO合成的改变；活性氧物质积累导致的心肌细胞凋亡^[21]；蛋白激酶C引起不依赖内皮的血管收缩^[22]；血浆内皮素-1水平升高^[23]

常见化疗药物类型	化疗药物名称	心脏毒性作用	分子机制
蒽环类药物	阿霉素、柔红霉素、表柔比星和伊达比星等	心肌细胞死亡；左心室功能障碍，最终降低心排血量^[7]	活性氧（reactive oxygen species，ROS）的生成与自身抗氧化作用的失衡^[8]；由拓扑异构酶Ⅱ与肿瘤结合引起的DNA双链裂解^[9]；细胞内钙超载^[10]； miRNA表达的上调损害心肌细胞线粒体^[11]；促进释放炎症因子^[12]；转化生长因子β信号的增强和肌成纤维细胞的激活^[13]
烷基化试剂	环磷酰胺	程序性细胞凋亡，导致心脏应激和心力衰竭^[14]	环磷酰胺在肝脏分解后产生的丙烯酰胺损害心肌细胞和内皮细胞；降低抗氧化剂的水平，导致心肌细胞中脂肪酸氧化的下调^[15]
铂类药物	顺铂	导致心肌细胞和血管内皮细胞受损，进而引起心肌细胞收缩功能障碍^[16]	扰乱细胞内氧化应激和抗氧化应激的平衡，导致氧自由基增加、DNA损伤和细胞凋亡^[17]
紫杉烷类	紫杉醇、多西他赛	轻度心肌损伤，表现为QT间期延长，心动过缓及心房心室纤维性颤动^[18]	促进微管蛋白聚合并抑制解聚，从而抑制肿瘤细胞形成纺锤体，进一步抑制有丝分裂进程，导致细胞周期停滞，抑制细胞增殖^[19]
代谢拮抗物	5-氟尿嘧啶、卡培他滨、替吉奥、TAS-102等	大部分可逆，导致冠状动脉血管痉挛和血管收缩^[20]	NO合成的改变；活性氧物质积累导致的心肌细胞凋亡^[21]；蛋白激酶C引起不依赖内皮的血管收缩^[22]；血浆内皮素-1水平升高^[23]

Research Progress on the Prevention and Treatment of Cardiotoxicity Caused by Chemotherapy Drugs

RichHTML

PDF

Knowledge

Abstract

Cite this article

share this article

Figures/Tables 1

References 72

Related Articles 3

Recommended Articles

Metrics

Comments

[1]	Jiayuan JIAO, Jiuge XING, Baoshan CHAI. Research Progress on RET Oncogene in Thyroid Carcinoma [J]. Current Biotechnology, 2023, 13(6): 895-899.
[2]	WANG Jue, HU Lili, LI Guilan, WU Na, ZHANG Yumin^*. Strategy for the Soluble Expression of the Astragalus membranaceus Pathogenesis-related Protein (AmPR-10) with Different Vectors of E. coli [J]. Curr. Biotech., 2021, 11(2): 231-237.
[3]	JIANG Hui1,2,3, LIU Yuqin1,2,3. The Epidemiological Situation, Prevention and Control of Tuberculosis Complicated with Diabetes Mellitus [J]. Curr. Biotech., 2017, 7(1): 25-29.