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Liu, J.; Chen, H.; Li, X.; Song, C.; Wang, L.; Wang, D. Effects of Natural Products on Lipid Metabolism Disorders. Encyclopedia. Available online: https://encyclopedia.pub/entry/48573 (accessed on 08 September 2024).
Liu J, Chen H, Li X, Song C, Wang L, Wang D. Effects of Natural Products on Lipid Metabolism Disorders. Encyclopedia. Available at: https://encyclopedia.pub/entry/48573. Accessed September 08, 2024.
Liu, Jinxin, Huanwen Chen, Xiaoli Li, Chunmei Song, Li Wang, Deguo Wang. "Effects of Natural Products on Lipid Metabolism Disorders" Encyclopedia, https://encyclopedia.pub/entry/48573 (accessed September 08, 2024).
Liu, J., Chen, H., Li, X., Song, C., Wang, L., & Wang, D. (2023, August 29). Effects of Natural Products on Lipid Metabolism Disorders. In Encyclopedia. https://encyclopedia.pub/entry/48573
Liu, Jinxin, et al. "Effects of Natural Products on Lipid Metabolism Disorders." Encyclopedia. Web. 29 August, 2023.
Effects of Natural Products on Lipid Metabolism Disorders
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This entry is adapted from the peer-reviewed paper 10.3390/molecules28176202

Natural products that are extracted from the source and from concentrated, fractionated, and purified yielding, which are generally defined as bioactive compounds, have the ability to modulate lipid metabolism, improve insulin signaling, and protect against cardiovascular damage.

natural products miRNAs lipid metabolism disorders

1. Introduction

Metabolic diseases, which encompass a variety of risk factors highly associated with obesity, diabetes, and cardiovascular diseases, have come to be regarded as public health challenges [1][2][3][4]. Due to their complex mechanisms of action, effective comprehensive treatments are still lacking. Even worse, the side effects of some curative drugs have been a major concern for their therapeutic usage [5][6][7]. Therefore, it is imperative to provide an effective treatment approach to overcome the aforementioned diseases.
Natural products that are extracted from the source and from concentrated, fractionated, and purified yielding, which are generally defined as bioactive compounds [8][9], have the ability to modulate lipid metabolism, improve insulin signaling, and protect against cardiovascular damage [10][11]. More importantly, natural products are widely distributed and readily available in nature [12]. To date, extensive studies have shown that plentiful drugs are derived from structural modification based on natural products [13]. MicroRNAs (miRNAs) and small noncoding RNAs are characterized by binding to the regulatory sites of 3′UTR of target mRNA, resulting in the inhibition of transcription or the promotion of degradation, accompanied by decreased protein synthesis [14][15]. Natural products could also ameliorate metabolic diseases by targeting abundant miRNAs [16][17][18]. Thus, the possibility for natural products to modify the abnormal patterns of these diseases is, at least in part, possible through a newly defined mechanism: the miRNAs cascade.

2. Effects of Natural Products on Lipid Metabolism Disorders

Lipid metabolism is a crucial and complex biochemical reaction in the body, and diseases caused by lipid metabolism disorders are common in modern society, such as obesity and hyperlipidemia [19]. Lipids are known to be important substances in energy storage and energy supply. Hence, the proper amount of adipose tissue is necessary for the human body. In general, however, patients have difficulty sticking to a long-term diet and physical activity regimen to combat these metabolic disorders. Therefore, food components that ameliorate the risk factors associated with these diseases can facilitate dietary-based therapies [16]. Dietary natural products have long been of great interest for improving lipid metabolism by modulating miRNA expression.

2.1. Regulatory Effects on Fatty Acid Synthesis and Decomposition

It is well known that fatty acids are the simplest type of lipids and are the building blocks of many more complex fats. Furthermore, they are also perceived as one of the main sources of energy on account of releasing a lot of energy during oxidation into CO2 and H2O in the case of a sufficient oxygen supply. Therefore, the role of fatty acids in the processes of lipogenesis and lipodieresis cannot be ignored. Recently, investigators have examined the regulatory effects of natural products on lipogenesis and lipodieresis, resulting in improved lipid metabolism through the management of diverse miRNAs (Table 1 and Table 2).
Table 1. The effects of natural products (extracts) on lipid metabolism disorders.
Natural Products (Extracts) Relevant miRNAs Dose Administration
Methods		 Experimental Models Targets Observed Effects References
Averrhoa carambola free phenolic extract miR-33↓
miR-34a↓		 10, 20, 30 g/kg/d for 8 weeks Gavage db/db mice / ● Reduced liver TG;
● Inhibited the signal transduction of hepatic lipogenesis;
● Exhibited a potent hepatic steatosis-relieving effect.		 [20]
Cerasus humilis polyphenol extract miR-7a/b↓ 40 μg/mL for 48 h;
250 g/kg/day for 12 weeks		 Cell culture;
gavage		 3T3-L1 pre-adipocyte cells; obese mice Sirt1, Prdm16 ● Reduced body weight;
● Improved abnormal serum lipid and glucose levels;
● Inhibited adipocyte differentiation;
● Reduced fat accumulation by mitigating fat deposition, inflammation, and oxidation.		 [21]
Citrus peel flavonoids miR-33↓
miR-122↓		 10 μg/mL for 0.5, 1, 3 and 6 h Cell culture Oleic acid-treated HepG2 cells FAS, CPT1a ● Attenuated intracellular lipid accumulation. [22]
Coffee polyphenols miR-122↑ 2.5 × 10−4%;
diet containing 0.5% or 1.0% coffee polyphenols for 15 weeks		 Cell culture;
diet		 Hepa 1-6 cells;
HFD-fed mice		 SREBP1c ● Activated AMPK;
● Enhanced energy metabolism;
● Reduced lipogenesis;
● Reduced body weight gain, abdominal and liver fat accumulation.		 [23]
Ginger extract miR-21↓
miR-132↓		 Diet containing 0.8% ginger extract for 10 weeks Diet HFD-fed rats / ● Lowered body weight and white adipose tissue mass;
● Reduced serum and hepatic lipid levels;
● Enhanced AMPK activity;
● Ameliorated obesity and inflammation.		 [24]
Grape seed proanthocyanidins extract miR-33a↓
miR-122↓		 5, 25, 50 mg/kg for 3 weeks Gavage HFD–induced obese rats ABCA1;
FAS, PPARβ/δ		 ● Hypolipidemic;
● Decreased total liver fat.		 [16]
miR-33a↓
miR-122↓		 5, 15, 25, 50 mg/kg for 3 weeks Gavage Healthy Wistar rats ABCA1;
FAS		 ● Improved postprandial hyperlipemia;
● Increased liver cholesterol efflux to HDL formation;
● Reduced fatty acid synthesis.		 [25]
miR-33↓
miR-122↓		 10, 25, 50, or 100 mg/L for 0.5, 1, 3, or 5 h;
250 mg/kg for 1 or 3 h		 Cell culture;
gavage		 FAO cells;
Wistar rats		 ABCA1;
FAS		 ● Hypolipidemic;
● Reduced lipogenesis;
● Increased liver cholesterol efflux to HDL formation.		 [26]
miR-33a↓
miR-122↓		 25 mg/kg for 3 weeks Gavage Dyslipidemic obese rats ABCA1, CPT1a;
FAS, PPARβ/δ		 ● Improved dyslipidemia;
● Decreased total liver fat.		 [27]
miR-96↓ 200 mg/kg/day for 180 days Diet HFD-fed mice mTOR, FOXO1 ● Decreased the weight gain, serum levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol but increased high-density lipoprotein cholesterol;
● Clearance of lipid accumulation.		 [28]
miR-33↓
miR-122↓		 250 mg/kg once Gavage HFD-fed grass carp / ● Decreased TG accumulation by reducing de novo lipogenesis and enhancing lipolysis and β-oxidation. [29]
Green tea extract miR-34a↓
miR-194↑		 500 mg/kg for 12 weeks (5 days/week) Gavage HFD-fed mice Sirt1, PPARα, INSIG2; HMGCS, APOA5 ● Protected against NAFLD development by altering lipid metabolism, increasing gene expression involved in triglycerides and fatty acid catabolism, and decreasing uptake and lipid accumulation. [30]
miR-335↓ 500 mg/kg for 12 weeks (5 days/week) Gavage HFD-fed mice FOXO1, GSK3β ● Reduced weight gain, adiposity and inflammation;
● Increased energy expenditure;
● Improved insulin sensitivity.		 [31]
Guarana extract miR-27b↓
miR-34b↓
miR-760↓		 150 µg/mL for 48 h Cell culture 3T3-L1 pre-adipocyte cells Wnt3a, Wnt1, Wnt10b ● Anti-adipogenic effect. [32]
Lychee pulp phenolics miR-33↓
miR-122↓		 500 mg/kg for 10 weeks Gavage HFD-fed mice ABCA1, ABCG1, NPC1;
FAS, ACC1, ACC2, SCD1, ACLY		 ● Hypolipidemic;
● Repressed fatty acid synthesis and promoting fatty acid β-oxidation and cholesterol efflux in the liver;
● Decreased body fat accumulation;
● Ameliorated lipid metabolism.		 [33]
Mulberry fruit extract miR-33↓ Diet containing 0.4% mulberry fruit extract for 4 weeks Diet High cholesterol/cholic acid diet-fed rats / ● Promoted serum high-density lipoprotein cholesterol levels;
● Decreased serum and hepatic cholesterol, serum low-density lipoprotein cholesterol, and fecal bile acid levels.		 [34]
Mulberry leaf extract miR-34a↓ 3 mg/mL for 24 h Cell culture Glucolipotoxicity-induced HepG2 cells Sirt1 ● Reduced liver fat accumulation;
● Decreased inflammatory responses and steatohepatitis;
● Exerted anti-glucolipotoxicity effects.		 [35]
Moringa oleifera leaf extract miR-21a↓
miR-103↓
miR-122↓
miR-34a↓		 9.375 mg/d for 8 weeks Gavage HFD-fed mice / ● Improved ITT and decreased SREBP1c hepatic protein, while Sirt1 increased;
● Reduced insulin resistance, de novo lipogenesis, hepatic inflammation, and ER stress;
● Prevented progression of liver damage in a model of NASH.		 [36]
Portulaca oleracea extract miR-122↓ 25, 50, 100 mg/kg/d for 7 days Gavage Acute alcoholic liver injury rats / ● Reduced the ethanol-elevated serum level of ALT, AST, ALP, and TG;
● Enhanced activities of SOD and GSH-Px;
● Decreased content of NO and MDA;
● Increased antioxidant capacity;
● Relieved the inflammatory injury;
● Improved the lipid metabolism disorder.		 [37]
miR-33↓
miR-34a↓		 Diet containing 0.8% portulaca oleracea L. extract for 4 weeks Diet High-cholesterol diet-fed rats / ● Improved serum, liver, and fecal lipid profiles;
● Promoted cholesterol efflux and bile acid synthesis;
● Enhanced hepatic AMPK activity.		 [38]
Rosmarinus officinalis extract miR let-7f-1↑ 30 μg/mL for 35 days Cell culture Human primary omental pre-adipocytes and adipocytes / ● Decreased triglyceride accumulation;
● Increased glycerol release;
● Stimulated lipolytic activity in differentiating pre-adipocytes and mature adipocytes;
● Modulated the adipocyte life cycle at different levels.		 [39]
The up arrow means an increase, and the down arrow means a decrease.
Table 2. The effects of natural products (compounds) on lipid metabolism disorders.
Natural Products (Compounds) Relevant miRNAs Dose Administration Methods Experimental Models Targets Observed Effects References
A-type ECG and EGCG dimers
Molecules 28 06202 i001		 miR-7a/b↑ ECG dimer: 20 μg/mL for 1–8 days;
ECGG dimer: 60 μg/mL for 1–8 days		 Cell culture 3T3-L1 pre-adipocyte cells PPARγ ● Inhibited pre-adipocyte differentiation;
● Reduced intracellular lipid accumulation;
● Blocked MCE process;
● Decreased the fluidity and hydrophobicity and increased the permeability of membrane.		 [40]
Curcumin
Molecules 28 06202 i002		 miR-17↓ 2 μM or 10 μM for 6 h; Cell culture 3T3-L1 pre-adipocyte cells;
HFD-fed mice		 TCF7L2 ● Inhibited adipocyte differentiation and adipogenesis;
● Stimulated the Wnt signaling pathway.		 [41]
Grape seed procyanidin B2
Molecules 28 06202 i003		 miR-483↓ 150 μg/mL for 48 h Cell culture 3T3-L1 pre-adipocyte cells PPARγ ● Inhibited pre-adipocyte differentiation;
● Reduced intracellular lipid accumulation.		 [42]
EGCG
Molecules 28 06202 i004		 miR-143↑ 50 μM for 24 h Cell culture 3T3-L1 pre-adipocyte cells MAPK7 ● Inhibited 3T3-L1 cell growth. [43]
Lycopene
Molecules 28 06202 i005		 miR-21↑ 50 μM for 24 h;
diet containing 0.05% lycopene for 8 weeks		 Cell culture;
gavage		 Hepa 1–6 cells;
HFD-fed mice		 FABP7 ● Lowered body weight;
● Inhibited intracellular lipid accumulation;
● Protected against HFD-induced hepatic steatosis.		 [44]
Nonivamide
Molecules 28 06202 i006		 miR let-7d↑ 1 μM for 12 days Cell culture 3T3-L1 pre-adipocyte cells PPARγ ● Impaired adipogenesis;
● Reduced mean lipid accumulation;
● Activated TRPV1.		 [45]
Oleanolic acid
Molecules 28 06202 i007		 miR-98↑ 10 mM for 6, 12, 24 h;
20 mg/kg for 4 weeks		 Cell culture HFD-fed mice;
db/db mice		 PGC1β ● Hypolipidemic. [46]
Persimmon tannin
Molecules 28 06202 i008		 miR-27↑ 20, 40, or 60 μg/mL for 1–8 days Cell culture 3T3-L1 pre-adipocyte cells PPARγ, C/EBPα ● Inhibited pre-adipocyte differentiation;
● Reduced intracellular lipid accumulation;
● Delayed MCE process.		 [47]
Pseudoprotodioscin
Molecules 28 06202 i009		 miR-33a/b↓ 25 μM for 24 h Cell culture Human HepG2 cells and THP-1 monocytic cells SREBP1c, SREBP2 ● Promoted the cholesterol effluxion. [48]
Resveratrol
Molecules 28 06202 i010		 miR-103↓
miR-107↓
miR-122↓		 30 mg/kg for 6 weeks Diet Obesogenic diet-fed rats SREBP1;
SREBP1, CPT1a;
FAS		 ● Reduced obesogenic diet-induced hepatic steatosis;
● Activated AMPK.		 [49]
miR-539↑ 30 mg/kg for 6 weeks Diet Obesogenic diet-fed rats SP1 ● Inhibited de novo lipogenesis. [50]
miR-155↑ 25 μM for 1–8 days Cell culture 3T3-L1 pre-adipocyte cells CEBP/α ● Inhibited adipogenesis. [51]
Zerumbone
Molecules 28 06202 i011		 miR-46b↓ 25 μM for 48 h;
diet containing 0.025% zerumbone for 8 weeks		 Cell culture;
diet		 3T3-L1 fibroblasts;
HFD-fed mice		 Sirt1 ● Induced AMPK activation and phosphorylation of acetyl-CoA carboxylase;
● Ameliorated diet-induced obesity and inhibited adipogenesis.		 [52]
The up arrow means an increase, and the down arrow means a decrease.
Specifically, miR-122 and miR-33 are two of the best-studied miRNAs involved in the regulation of lipid metabolism [53]. As is shown in Table 1 and Table 2, numerous pieces of evidence have revealed that grape seed proanthocyanidin extract treatments reduced fatty acid synthesis and de novo lipogenesis, increased liver cholesterol efflux to high-density lipoprotein (HDL) formation by decreasing the expression of miR-122 and miR-33, which could regulate several genes that control fatty acid and transcriptional regulatory factors, such as fatty acid synthase (FAS) and peroxisome proliferator-activated receptor beta/delta (PPARβ/δ), as well as genes that regulate fatty acid β-oxidation, such as ATP-binding cassette transporter A1 (ABCA1) and carnitine palmitoyltransferase 1a (CPT1a), respectively [16][25][26][27][29][54]. Further detection revealed that the levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) were reduced while the level of high-density lipoproteins cholesterol (HDL-C) was enhanced in a dose-dependent manner [16][25][26][27]. Averrhoa carambola-free phenolic extract, citrus peel flavonoids, lychee pulp phenolics, mulberry fruit extract, and portulaca oleracea extract treatments could also improve lipid metabolism in in vitro and in vivo studies; the underlying mechanism was miR-33 or miR-122-mediated changes in the signaling pathways [20][22][33][34][37][38]. However, the opposite expression of miR-122 was reflected in a natural product experiment using coffee polyphenols, which could enhance energy metabolism and reduce lipogenesis by targeting sterol regulatory element binding protein (SREBP) 1c mediated by miR-122 [23]. Accountably, SREBP1c, one of the three isoforms of SREBPs, comes into play in fatty acid synthesis and metabolism [55][56]. It potentially illustrates the point that the same type of miRNAs can act on a variety of target genes with different expressions. Similarly, the same target gene may also be regulated by multiple miRNAs. Recent studies have shown that miR-103 and miR-107 reduced obesogenic diet-induced hepatic steatosis via decreasing the protein expression of SREBP1 in resveratrol-treated rats [49], and pseudoprotodioscin promoted cholesterol effluxion through targeting SREBP1c and SREBP2 mediated by miR-33a/b in an in vitro experiment [48]. In addition, distinctively, the overexpression of hepatic miR-98 induced by oleanolic acid, an active component of the traditional Chinese herb olea europaea, increased the degradation of peroxisome proliferator-activated receptor gamma coactivator-1beta (PGC1β), known as a transcriptional co-activator of SREBP-1 and the master regulator of hepatic lipogenesis [46][57].
Intuitively, both FAS and SREBP1 are involved in the process of fatty acid synthesis, and the connection between them is found in the following experiments. SP1 transcription factor (SP1), an important member of the ubiquitously expressed SP/KLF transcription factor family, acts together with SREBP1 to synergistically activate the promoter of the FAS gene and is involved in de novo lipogenesis [58]. Hence, resveratrol reduced the expression of SP1 through upregulating miR-539, along with decreasing the expression of the SREBP1 protein and FAS gene in vivo and in vitro [50]. Nevertheless, the correlation between them still needs to be systematically and intensively investigated beyond all doubt.
Lipid metabolism is a complex process, and natural products can regulate lipogenesis and lipodieresis in a variety of ways. Zerumbone is a cyclic sesquiterpene isolated from the wild ginger Zingiber zerumbet smith. It has been proved that zerumbone could improve lipid metabolism disorder by reducing lipogenesis and increasing fatty acid oxidation [52]. For one thing, zerumbone acted as a miR-146b inhibitor and downregulated miR-146b, leading to the activation of sirtuin type 1 (Sirt1), which induced the de-acetylation of forkhead box O1 (FOXO1) and peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC1α); for another, zerumbone induced the phosphorylation of AMP-activated protein kinase (AMPK), which could limit fatty acid efflux from adipocytes and favor fatty acid oxidation, as well as decrease de novo fatty acid synthesis through the phosphorylation-mediated inhibition of acetyl-CoA carboxylase (ACC) [59][60][61] and also activated Sirt1 indirectly [52]. With these similar natural product experiments, miR-27a/b, miR-96, miR-34a, miR-194, and miR-355 also participated in the process of lipid metabolism by targeting Sirt1 or FOXO1, which could both increase energy expenditure and the clearance of lipid accumulation [21][28][30][31][35][36]. And ginger extract could enhance AMPK activity and ameliorate obesity and inflammation by regulating miRNAs expressions in high-fat diet (HFD)-fed rats [24].
Based on the present studies, regulating miRNAs is potentially becoming a dominant feature in terms of natural products regulating lipid metabolism (Figure 1). On the one hand, it can inhibit fatty synthesis by reducing fatty acid synthesis and increasing fatty acids mobilization. On the other hand, it can also accelerate lipodieresis by enhancing the oxidation and phosphorylation of fatty acids.
Figure 1. Schematic illustration of the main mechanisms by which natural products improve lipid metabolism disorders mediated by miRNAs. The red arrow means an increase, and the green arrow means a decrease.

2.2. Inhibitory Effects on Adipocyte Differentiation and Accumulation

From the perspective of the cellular level, however, the growth of adipose tissue is the result of an increase in the number of adipocytes and the volume of individual cells [51]. The former contributes to promoting pre-adipocyte differentiation into mature adipocytes, whereas the latter is due to lipid accumulation. The functional role of natural products in this regard, as well as their potential mechanisms of action was summarized  (Figure 1 and Table 1 and Table 2).
Adipocyte differentiation is a highly precisely regulated cellular process. Ahead of terminal differentiation, the mitotic clonal expansion (MCE) of stimulated pre-adipocytes is an essential procedure in adipocyte differentiation. Moreover, the transcriptional activation of adipocyte-specific functional genes is closely related to their differentiation [62]. 3T3-L1 pre-adipocytes have long been considered as the “gold standard” for investigating pre-adipocyte differentiation in vitro [63][64]. There has been evidence that the MCE process could be delayed by persimmon tannin by enhancing the expression of miR-27 in 3T3-L1 pre-adipocytes [47]. Furthermore, multiple transcriptional factors, including peroxisome proliferator-activated receptor-gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) were also attenuated by miR-27, resulting in a decrease in adipocyte-specific genes, such as adipocyte fatty acid binding protein (aP2) and lipoprotein lipase (LPL). Similarly, the MCE process was blocked by miR-27a/b in the study of a-type ECG and EGCG dimers [40]. Lipids are important structural components in cell membranes [65]. Notably, with different molecular structures, a-type ECG and EGCG dimers strongly disturbed the structures of cell membranes by decreasing fluidity and hydrophobicity and increasing the permeability of the membrane of 3T3-L1 pre-adipocyte cells, thus displaying significant inhibition on differentiation [40]. EGCG also suppressed 3T3-L1 cell growth via miR-143/MAPK7 pathways [43]. Nonivamide-induced reduction in lipid accumulation was mediated by transient receptor potential cation channel subfamily V member 1 (TRPV1) activation [45]. Although miRNAs are involved in the adipocyte differentiation process, whether they affect membrane structure remains to be intensively studied in natural product therapy.
The activation of C/EBPα and PPARγ is not only necessary for adipocyte differentiation in the early stage but is also crucial for terminal adipocyte differentiation [66]. The evidence suggests that grape seed procyanidin B2 could inhibit pre-adipocyte differentiation and reduce intracellular lipid accumulation by modulating the miR-483/PPARγ axis [42]. Resveratrol reduced the expression of CEBP/α by boosting miR-155, resulting in decreasing lipogenesis [51]. Consistent with these, as shown in Table 2, similar results were also obtained in the research of lycopene by regulating the expression of miR-21 [44]. What is noteworthy is that accompanied with the involvement of multiple miRNAs, Rosmarinus officinalis extract significantly reduced triglyceride incorporation during pre-adipocyte maturation in a dose-dependent manner and decreased the expression of cell cycle genes, such as cyclin-dependent kinase 4, cyclin D1, and cyclin-dependent kinase inhibitor 1A [39]. The final and most studied phase of adipocyte differentiation involves terminal differentiation and the induction of a signaling cascade to promote the expression of the genes necessary for adipocyte function [67][68]. The canonical Wnt signaling cascade is an effective approach to suppress adipogenesis [69][70][71]. Recently, investigators found that curcumin repressed 3T3-L1 pre-adipocyte cell adipogenic differentiation by inhibiting the expression of miR-17 and stimulating transcription factor 7-like 2 (TCF7L2), which is the Wnt signaling pathway effector and a direct downstream target of miR-17 [41]. And guarana extract also exerted an anti-adipogenic effect by regulating the Wnt signaling pathway, mediated by miRNAs [32]. In summary, natural products may inhibit adipocyte differentiation and accumulation by regulating miRNAs, which play a crucial role in the process of lipogenesis.

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Subjects: Endocrinology & Metabolism
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Jinxin Liu
,
Huanwen Chen
,
Xiaoli Li
,
Chunmei Song
,
Li Wang
,
Deguo Wang
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Revisions: 2 times (View History)
Update Date: 30 Aug 2023
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