Neprilysin Inhibition in the Prevention of Anthracycline-Induced Cardiotoxicity
Abstract
:Simple Summary
Abstract
1. Introduction
2. AIC Characteristics
3. Molecular Mechanisms of AIC
4. Prevention of AIC
5. Neprilysin Inhibition in HF
6. ARNi in Preclinical Models of Myocardial Infarction
7. ARNi in Preclinical Models of Other CVDs
8. ARNi in Preclinical Models of AIC
9. ARNi in Human Studies on AIC
10. Summary and Future Perspectives
11. Conclusions
Supplementary Materials
Author Contributions
Funding
Conflicts of Interest
References
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Paper by | Animal Model | Gavage Initiation | Groups | LVEF (%) | Other Findings | |
---|---|---|---|---|---|---|
Chang [89] | SPRD rats | 1 wk after MI | Vehicle Enalapril ARNi | 38.5 ± 2.0 46.7 ± 9.1 ↑ 57.6 ± 5.5 ↑↑ | ↓↓ HW/BW ratio in ARNi ↓↓ Ventricular arrhythmias inducibility in ARNi ↑↑ Expression of K+ channel proteins in ARNi | |
Chang [90] | New Zealand White rabbits | 1 wk after MI | Vehicle ARB ARNi | 37.1 ± 6.3 44.3 ± 6.3 ↑ 53.8 ± 10.0 ↑↑ | ↓↓ Ventricular arrhythmia inducibility in ARNi | |
Ishii [91] | Mice | 1 day after MI | Vehicle Enalapril ARNi | NA | ↓↓ Post-MI mortality rate due to LV rupture in ARNi ↑↑ %FS 14 and 28 days post-MI in ARNi ↓↓ Myocardial expression of IL1β, IL6, and MMP-9 mRNA in ARNi No differences in myocardial fibrosis and inflammatory infiltration. | |
Kompa [92] | SPRD rats | 1 wk after MI | Vehicle Perindopril ARNi | 40.46 ± 1.27 42.22 ± 1.16 46.65 ± 0.83 ↑↑ | ARNi improved end-systolic pressure-volume relationship compared with perindopril ↓ LV mass, cardiomyocyte CSA, and cardiac fibrosis in perindopril and ARNi ↓↓ ANP, MHC β, and TIMP2 expression in ARNi | |
Liu [93] | C57BL/6J mice | Directly after MI | Vehicle Benazepril ARNi ARNi + Benazepril | = 58.7 ± 0.42 ↑ 62.35 ± 0.25 ↑↑ | HW/BW ratio ↓ in ARNi and benazepril and ↓↓ in ARNi + benazepril Myocardial fibrosis ↓ in ARNi and ↓↓ in ARNi + benazepril ↓↓ TGFβ1 expression in ARNi and ARNi + benazepril No differences in IL6 and TNFɑ expression. | |
Pfau [94] | Lewis rats | 1 wk after MI | Vehicle ARB ARNi | 1 wk: 34 ± 2 38 ± 2 39 ± 2 ↑ | 5 wks: 35 ± 2 39 ± 2 42 ± 2 | ↓ HW/TL ratio and fibrosis in ARNi ↓ Myocyte CSA in ARNi and ARB ↓ Expression of CTGF, MHCβ, MHCβ/α, and ANP in ARNi and ARB |
Raj [95] | SPRD rats | Directly after MI | Vehicle ARB ARNi | 56.60 ± 1.70 65.45 ± 2.70 ↑ 66.82 ± 1.43 ↑ | ↓ Oxidative stress in ARNi and ARB ↓ TNFα, collagen, and BNP in ARNi and ARB | |
Shen [96] | SPRD rats | 1 wk after MI | Vehicle ARNi | 3 days: ↑ | 7 days: ↑ | ↓ Interstitial fibrosis in ARNi ↓ Serum IL1βa and IL18 levels in ARNi ↓ ROS and NLRP3 inflammasome activation in ARNi |
Suematsu [97] | C57BL/6J diabetic mice | Day after MI | Vehicle ARB ARNi | 29 ± 3.2 = 43 ± 3.4 ↑ | ↓↓ LV fibrosis and expression of TGFβ mRNA in ARNi ↓ HW/BW ratio in ARB and ARNi ↓ ANP mRNA in ARNi | |
Torrado [98] | New Zealand White rabbits | At reperfusion only | Vehicle ARB ARNi | ARB = ARNi ↑ | ↓ Infarct size in ARB and ARNi and ↓ cardiac troponin I serum concentration in ARNi | |
At LVEF ≤ 40% | ARB = ARNi ↑↑ | |||||
At reperfusion | 4 wks: ARB = ARNi ↑↑ | 10 wks: = ↑ | ↓ Infarct size in ARNi | |||
Trivedi [99] | SHRs | 4 wks after reperfusion | Vehicle ARB ARNi | = = ↑↑ | ↓ Infarct border zone expansion in ARB and ARNi Aortic vasorelaxation responses to Ach and SNP ↑ in ARB and ↑↑ in ARNi ↑↑ Myocardial NO bioavailability in ARNi No differences in fibrosis between groups | |
Vaskova [100] | SPRD rats | 1 wk after MI | Vehicle ARB ARNi | 36.79 ± 2.1 40.68 ± 4.8 ↑ 41.42 ± 3.4 ↑ | ↑ Production of plasma exosomes in ARB and ARNi ↓↓ Expression of rno-miR-181a in ARNi ↓ Fibrosis in ARB and ARNi | |
Von Lueder [101] | Lewis rats | 1 wk after MI | Vehicle ARNi | 47 ± 5 60 ± 2 ↑ | Improved LV function in pressure-volume loops in ARNi ↓ LV mass and fibrosis in peri-infarct and remote myocardium in ARNi No differences in infarct size and perivascular fibrosis. |
Model of | Paper by | Species | Gavage Initiation | Groups | Findings * |
---|---|---|---|---|---|
HFpEF due to pressure overload | Burke [103] | C57Bl6/J mice | A day before TAC, cont. for 4 wks | Vehicle ARB ARNi | ↑↑ LVEF in ARNi ↓↓ Interstitial fibrosis and fibroblast population in ARNi ↓↓ Cardiomyocyte CSA and HW/TL in ARNi |
Lu [108] | SPRD rats | 4 wks after TAC, cont. for 32 days | Vehicle Enalapril ARNi | ↓↓ Sarcomere-length, left ventricle fibrotic area, cardiomyocyte size and lung injury in ARNi ↓↓ Expressions of fibrotic, oxidative, apoptotic, DNA damage, mitochondrial damage, volume overload markers in LV in ARNi | |
Norden [111] | SPRD rats | Cont. for 8 wks | Vehicle ARB ARNi | ↓↓ LV weight in ARNi ↓↓ Diastolic dysfunction in ARNi No differences in LVEF and myocardial fibrosis | |
Suo [115] | C57BL/6J mice | 8 wks after TAC, cont. for 4 wks | Vehicle ARB ARNi | ↑↑ LVEF in ARNi ↓↓ Fibrosis in ARNi | |
HT | Hamano [104] | SHRcp fed high-salt diet | I: 6 mos, with high-salt diet | Vehicle ARB ARNi | ↓ LV/BW ratio in ARNi in Plan I ↓↓ LV/BW and pulmonary edema in ARB in Plan II No differences in cardiomyocyte CSA and fibrosis |
II: After 6 mos of high-salt diet, cont. for 6 mos | |||||
Kusaka [105] | SHRcp fed high-salt diet | Cont. for 4 wks | Vehicle ARB ARNi | ↓ LV in ARNi ↓↓ Myocardial fibrosis in ARNi ↓↓ Impairment of acetylcholine-induced vascular relaxation in ARNi | |
Seki [112] | SHRs | Cont. for 12 wks | Vehicle ARB ARNi | Endothelium-dependent hyperpolarization-mediated responses improved similarly in ARB and ARNi ↓ LV in ARNi | |
Sung [114] | SHRs | Cont. for 2 wks | Vehicle ARB ARNi | ↓↓ Diastolic dysfunction and ↓↓ ventricular hypertrophy in ARNi ↓↓ Incidence of ventricular arrhythmias in ARNi No differences in LVEF | |
Tashiro [116] | C57BL/6J mice | Started on the 7th day of Ang II infusion, cont. for 2 wks | Vehicle Enalapril ARB ARNi | ↓↓ LV concentric hypertrophy in ARNi Myocyte CSA ↓ in ARB, ↓ in enalapril, and ↓↓ in ARNi No differences in fibrosis and TGFβ expression | |
Zhao [117] | SHRs | Cont. for 12 wks | Vehicle ARB ARNi | LVEF ↑↑ in ARNi and ↑ in ARB ↓↓ LV mass in ARNi ↓ Fibrosis, TGFβ expression and nNOS, eNOS protein expression in ARB and ARNi ↓↓ ACE, ATR1, and ↑↑ ACE2, MasR, ATR2 cardiac protein expression in ARNi | |
HF due to volume overload (by AVI) | Maslow [109] | SPRD rats | 4 wks after AVI, cont. for 4 wks | Vehicle ARB NEPi ARNi | Improved load-dependent indexes of left ventricle contractility and relaxation only in ARNi Improved load-independent index of contractility in ARB and ARNi ↑↑ Exercise tolerance in ARNi ↓↓ Myocardial fibrosis in ARNi |
Maslow [110] | SPRD rats | On the day of AVI, cont. for 8 wks | Vehicle ARB NEPi ARNi | ↑ LVEF in ARNi ↓ Myocardial fibrosis in ARB, NEPi, and ARNi ↑ Exercise tolerance in ARB and ARNi | |
HFpEF due to obesity | Aroor [102] | Zucker Obese rats | At 16 wks of age, cont. for 10 wks | Vehicle ARB ARNi | ↑ LVEF, ↓ fibrosis, and ↓ oxidative stress in ARB and ARNi ↑ Endothelial-dependent aortic relaxation in ARB and ARNi ↑↑ E’/a’ ratio in ARNi |
AF | Li [106] | SPRD rats | After AF induction, cont. for 4 wks | Vehicle ARB ARNi | ↑ LVEF in ARB and ARNi ↓↓ Atrial fibrosis and susceptibility to AF in ARNi |
Myocarditis | Liang [107] | BALB/c mice | On the day of myocarditis, cont. for 3 wks | Vehicle ARB ARNi | ↓↓ HW/BW ratio, ↓↓ myocardial histopathologic scores, and ↓↓ cTnT levels in ARNi ↓↓ Serum hsCRP, IL6, and serum/myocardial IL17 levels in ARNi ↓↓ Th17 cells and their transcription factors in myocardial tissue in ARNi |
CKD | Suematsu [113] | SPRD rats | 2 wks after nephrectomy, cont. for 8 wks | Vehicle ARB ARNi | HW/BW ratio, myocyte CSA, markers of oxidative stress, myocardial and aortic fibrosis ↓↓ in ARNi and ↓ in ARB ↓↓ expression of NF-κB, COX-2 in ARNi |
Paper by | Animal Model | Groups + Dosage (mg/kg/d) | Other Findings (Presented in Comparison to DOX + Vehicle Groups) |
---|---|---|---|
Boutagy [127] | Wistar rats | DOX + Vehicle DOX + ARB 31 DOX + ARNi 68 | ↑ LVEF in ARNi ↓ Myocyte vacuolation in ARNi and ARB ↓ Myocardial fibrosis in ARNi and ARB at 4 wks (no longer seen at 6 wks) ↓ Capillary density in ARNi at 6 wks ↓ Matrix metalloproteinases activity in ARNi at 4 wks ↓ Myocyte CSA and heart weight in all DOX-receiving groups No differences in cellular apoptosis between groups |
Dindas [128] | Balb-c mice | Vehicle ARNi 80 DOX + Vehicle DOX + ARNi 80 | ↓ Degenerative changes and streaking in cardiomyocytes in DOX + ARNi ↓ QRS duration, ST interval and QT/PQ index in DOX + ARNi ↓ NT-proBNP, TNFα, IL1β, IL6, and caspase 3 in DOX + ARNi ↓ Total oxidant status and ↑ total antioxidant status in DOX + ARNi |
Kim [129] | Sprague Dawley rats | Vehicle DOX + Vehicle DOX + ARNi 60 | ↓ Cardiomyocyte apoptosis in ARNi ↓ Endoplasmic reticulum stress in ARNi ↓ Serum cardiac troponin I and NT-proBNP levels in ARNi group |
Maurea [133] | C57Bl/6 mice | Sham Sac/Val 60 DOX DOX + Sac/Val 60 | ARNi improved EF and prevented the reduction of radial and longitudinal strain ↓ Cardiac expression of NLRP3, MyD88, DAMPs, and NF-kB in ARNi ↑ Expression of phosphorylated AMPK in ARNi ↓ Levels of Calgranulin S100 and galectine-3 in ARNi |
Miyoshi [130] | Sprague Dawley rats | DOX + Vehicle DOX + Val 31 DOX + ARNi 68 | No differences in LVEF and FS between groups. ↑ Cardiomyocyte CSA and ↑ cardiac fibrosis in ARNi ↑ Cardiac TNFα and ANP mRNA expression in ARB and ARNi ↓ Myocardial collagen I mRNA expression in ARNi ↓ Cardiac troponin T and NT-proBNP levels in ARNi ↓ Cardiac reactive oxygen species levels in ARNi ↑ Phosphorylation of AMPK and ↑ Bax/Bcl-2 ratio in ARNi |
Xia [131] | Balb-c mice | Vehicle DOX + Vehicle DOX + ARNi 80 | ↓ Cardiac hypertrophy, myocardial fibrosis and cellular apoptosis in ARNi ↓ Heart weight/body weight and ↑ heart weight/tibial length in ARNi ↑ Single cardiomyocyte contractile function in ARNi ↓ Pathologic changes to mitochondria and ↓ Drp1 expression in ARNi ↓ Cleaved caspase 3 in ARNi |
Ye [48] | C57BL/6 mice | Vehicle DOX + Vehicle DOX + ARNi 60 TLR2 KO + Vehicle TLR2 KO + DOX | ↑ LVEF in ARNi, TLR2 KO, and TLR2 KO + DOX ↓ Ventricular wall thinning and ↓ heart cavity enlargement in ARNi and TLR2 KO ↓ Myocardial fibrosis in ARNi and TLR2 KO ↓ Myocardial collagen I and TGFβ protein levels in ARNi and TLR2 KO ↓ Myocardial TNFα and NF-κB levels in ARNi and TLR2 KO |
Yu [132] | New Zealand white rabbits | Vehicle DOX + Vehicle DOX + ARNi 5 DOX + ARNi 10 | ↓ PR segment, QRC segment prolongation, QT interval and QT/PQ index in both ARNi groups ↓ Serum BNP level in ARNi groups ↑ Activity of superoxide dismutase and catalase and ↓ lipid peroxidation in both ARNi groups |
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Sobiborowicz-Sadowska, A.M.; Kamińska, K.; Cudnoch-Jędrzejewska, A. Neprilysin Inhibition in the Prevention of Anthracycline-Induced Cardiotoxicity. Cancers 2023, 15, 312. https://doi.org/10.3390/cancers15010312
Sobiborowicz-Sadowska AM, Kamińska K, Cudnoch-Jędrzejewska A. Neprilysin Inhibition in the Prevention of Anthracycline-Induced Cardiotoxicity. Cancers. 2023; 15(1):312. https://doi.org/10.3390/cancers15010312
Chicago/Turabian StyleSobiborowicz-Sadowska, Aleksandra M., Katarzyna Kamińska, and Agnieszka Cudnoch-Jędrzejewska. 2023. "Neprilysin Inhibition in the Prevention of Anthracycline-Induced Cardiotoxicity" Cancers 15, no. 1: 312. https://doi.org/10.3390/cancers15010312
APA StyleSobiborowicz-Sadowska, A. M., Kamińska, K., & Cudnoch-Jędrzejewska, A. (2023). Neprilysin Inhibition in the Prevention of Anthracycline-Induced Cardiotoxicity. Cancers, 15(1), 312. https://doi.org/10.3390/cancers15010312