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Cited by 10Renal Diseases and GlomerulopathiesChronic Kidney Disease and DiabetesLipid metabolism and disorders

Lipoprotein glomerulopathy induced by ApoE Kyoto mutation in ApoE-deficient mice

Open access
Wu, Hongyan, Yang, Jing, Liu, Yun-Qiang, Lei, Song, Yang, Mei, Yang, Zhi, Yang, Yuan, Hu, Zhangxue·2021·Journal of Translational Medicine
DOI 10.1186/s12967-021-02765-xPMC PMC7934380

Published version of a preprint

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Abstract

Background: Lipoprotein glomerulopathy (LPG) is a rare autosomal dominant kidney disease that is most commonly caused by mutations in ApoE Kyoto (p.R43C) and ApoE Sendai (p.R163P). Differences in phenotype among the various ApoE mutations have been suggested, but the pathogenic role of ApoE Kyoto has not been validated in an animal model. This study intended to establish an ApoE Kyoto murine model and to further compare the pathologic differences between ApoE Kyoto and ApoE Sendai. Method: Male ApoE-deficient mice, 3 months of age, were divided into five groups, including the AD-ApoE Sendai, AD-ApoE Kyoto, AD-ApoE3, AD-eGFP, and ApoE (−/−) groups. The first four groups received recombinant adenovirus that contained the entire coding regions of the human ApoE Sendai and ApoE Kyoto , apoE3 , and eGFP genes, respectively. Fasting blood and urine samples were collected at multiple time points. Lipid profiles and urine albumin–creatinine ratio were measured. Renal and aortic histopathologic alterations were analyzed. Results: After virus injection, plasma human ApoE was detected and rapidly reached the maximum level at 4–6 days in the AD-ApoE Kyoto and AD-ApoE Sendai groups (17.4 ± 3.1 µg/mL vs.: 22.2 ± 4.5 µg/mL, respectively) and at 2 days in the AD-ApoE3 group (38.4 µg/mL). The serum total cholesterol decreased by 63%, 65%, and 73% in the AD-ApoE Kyoto, AD-ApoE Sendai and AD-ApoE3 groups, respectively. There were no significant changes in serum triglyceride and urinary albumin–creatinine ratio among the five groups. Typical lipoprotein thrombi with positive ApoE staining were detected in the AD-ApoE Kyoto and AD-ApoE Sendai groups. The Oil-red O-positive glomerular area tended to be higher in the AD-ApoE Kyoto group (9.2%) than in the AD-ApoE Sendai (3.9%), AD-ApoE3 (4.8%), AD-eGFP (2.9%), and ApoE (−/−) (3.6%) groups. The atherosclerotic plaque area in the aorta was lower in the group injected with various ApoE mutations than in the group without injection of ApoE mutation. Conclusions: In this animal study, we first established an ApoE Kyoto mutation murine model and confirmed its pathogenic role in LPG. Our results suggested that LPG may be more severe with the ApoE Kyoto than with the ApoE Sendai.

AI snapshot

Written from the paper’s full text.

TL;DR

This study established an ApoE Kyoto murine model of lipoprotein glomerulopathy (LPG) using adenovirus-mediated expression in ApoE-deficient mice and confirmed its pathogenic role. The results suggest LPG may be more severe with ApoE Kyoto than with ApoE Sendai, while ApoE mutations still appeared to protect against atherosclerosis.

Key findings

  • LPG-like renal lesions were observed in 3 mice of the AD-ApoE Kyoto group and 1 mouse of the AD-ApoE Sendai group; lipoprotein thrombi were positive for ApoE and Oil-red O and contained osmiophilic granules and lipid vacuoles on electron microscopy.
  • Plasma human ApoE peaked at 17.4 ± 3.1 µg/mL in AD-ApoE Kyoto and 22.2 ± 4.5 µg/mL in AD-ApoE Sendai at 4–6 days, and at 38.4 µg/mL in AD-ApoE3 at 2 days. Serum total cholesterol decreased by 63%, 65%, and 73% in the AD-ApoE Kyoto, AD-ApoE Sendai, and AD-ApoE3 groups, respectively; serum triglyceride and urinary albumin–creatinine ratio showed no significant changes among the five groups.
  • The Oil-red O-positive glomerular area was 9.2% in AD-ApoE Kyoto, compared with 3.9% in AD-ApoE Sendai, 4.8% in AD-ApoE3, 2.9% in AD-eGFP, and 3.6% in ApoE (−/−); there was no difference in the percentage of Oil-red O-positive glomeruli among groups.
  • Atherosclerotic plaque area was lower in the ApoE mutation groups than in non-ApoE-injected groups: 0.18 ± 0.05 × 10⁶ µm² for AD-ApoE Kyoto, 0.16 ± 0.06 × 10⁶ µm² for AD-ApoE Sendai, and 0.13 ± 0.06 × 10⁶ µm² for AD-ApoE3, versus 0.25 ± 0.1 × 10⁶ µm² for AD-eGFP and 0.27 ± 0.15 × 10⁶ µm² for ApoE (−/−).

Methods

  • Male ApoE (−/−) mice on a C57BL/6 background, 3 months old and on normal chow, were randomly divided into five groups: AD-ApoE Sendai (n = 6), AD-ApoE Kyoto (n = 6), AD-ApoE3 (n = 6), AD-eGFP (n = 5), and ApoE (−/−) (n = 4). The first four groups received recombinant adenovirus containing human ApoE Sendai, ApoE Kyoto, apoE3, or eGFP coding regions.
  • Blood and urine were collected at baseline and 2, 4, 6, 10, 14, 20, 34, 50, 65, and 90 days after injection. Plasma total cholesterol and triglyceride were measured enzymatically, human ApoE by sandwich ELISA, and urine albumin–creatinine ratio calculated. Kidneys were analyzed after 90 days by hematoxylin/eosin, periodic acid-Schiff, ApoE immunofluorescence, Oil-red O, and electron microscopy; aortic valve atherosclerosis was assessed by Oil-red O.
  • Data are presented as mean ± SD and compared by one-way analysis of variance, with significance at p < 0.05.

Limitations

  • The paper states that the number of animals was small and that LPG’s incomplete penetrance made statistical analysis difficult, especially for comparing the two pathogenic ApoE variants; a larger sample size was needed.
  • The text also makes evident that adenovirus-mediated ApoE expression lasted only 7–10 days and then declined, unlike sustained ApoE mutant expression in human LPG; the affected glomeruli rate was fairly low, macrophage function appeared intact, and normal chow may have contributed to low penetrance.
  • The normal urinary albumin–creatinine ratio in the ApoE variant groups suggested the model reflected an early stage of LPG.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1186/s12967-021-02765-x

Cites

21 of 21 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

5 of 15 cited sources checked · 4 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    A majority of animal experiments suggested that human apoE3 could postpone the progression of atherosclerosis by decreasing serum total cholesterol or changing the inflammatory cell composition of the local plaque.

    “A majority of animal experiments suggested that human apoE3 could postpone the progression of atherosclerosis by decreasing serum total cholesterol or changing the inflammatory cell composition of the local plaque [19–21].”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [19] Tavori H, Fan D, Giunzioni I, Zhu L, Linton MF, Fogo AB, et al. Macrophage-derived apoESendai suppresses atherosclerosis while causing lipoprotein glomerulopathy in hyperlipidemic mice. J Lipid Res. 2014;55(10):2073–81. source
    • cites [20] Kitajima K, Marchadier DH, Miller GC, Gao GP, Wilson JM, Rader DJ. Complete prevention of atherosclerosis in apoE-deficient mice by hepatic human apoE gene transfer with adeno-associated virus serotypes 7 and 8. Arterioscler Thromb Vasc Biol. 2006;26(8):1852–7. source
    • cites [21] Osman E, Evans V, Graham IR, Athanasopoulos T, McIntosh J, Nathwani AC, et al. Preliminary evaluation of a self-complementary AAV2/8 vector for hepatic gene transfer of human apoE3 to inhibit atherosclerotic lesion development in apoE-deficient mice. Atherosclerosis. 2009;204(1):121–6. source
  • Premisecitation

    Patients with LPG and mild hyperlipidemia have been reported clinically.

    “patients with LPG and mild hyperlipidemia have been reported clinically [5, 15].”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [5] Tokura T, Itano S, Kobayashi S, Kuwabara A, Fujimoto S, Horike H, et al. A novel mutation ApoE2 Kurashiki (R158P) in a patient with lipoprotein glomerulopathy. J Atheroscler Thromb. 2011;18(6):536–41. source
    • cites [15] Mitani A, Ishigami M, Watase K, Minakata T, Yamamura T. A novel apolipoprotein E mutation, ApoE Osaka (Arg158 Pro), in a dyslipidemic patient with lipoprotein glomerulopathy. J Atheroscler Thromb. 2011;18(6):531–5. source
  • Findingown data

    Typical lipoprotein thrombi with positive ApoE staining were detected in the AD-ApoE Kyoto and AD-ApoE Sendai groups.

    “Typical lipoprotein thrombi with positive ApoE staining were detected in the AD-ApoE Kyoto and AD-ApoE Sendai groups.”
    • Also stated in: § Histologic manifestation of renal lesions · plain
      “Lipoprotein thrombi were observed in the dilated capillary lumina and mesangial area of the glomeruli by toluidine blue staining and were positive for ApoE and Oil-red O staining.”
    Quote in the paperSubstantial claim
  • Findingown data

    Atherosclerotic plaque area in the aorta was lower in groups injected with various ApoE mutations than in groups without injection of ApoE mutation.

    “The atherosclerotic plaque area in the aorta was lower in the group injected with various ApoE mutations than in the group without injection of ApoE mutation.”
    • Also stated in: § Analysis of atherosclerosis in the aortic valve · plain
      “Atherosclerosis progression was slower in the three groups that were injected with various ApoE variants than in the other two groups.”
    • Also stated in: § Discussion · plain
      “we found that the atherosclerotic plaque area was lower in the ApoE mutant groups than in the ApoE-deficient mice”
    Quote in the paperSubstantial claim
  • Findingown data

    There was no significant difference in ApoE peak concentration between the AD-ApoE Kyoto and AD-ApoE Sendai groups.

    “There were no significant differences in the ApoE peak concentration between the AD-ApoE Kyoto and AD-ApoE Sendai groups.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim. 6
  • May combine two claims. 13

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Patients with LPG with mutations in the LDL receptor binding region have relatively high blood pressure and serum ApoE levels.

    “patients with LPG with mutations in the LDL receptor binding region were reported to have relatively high blood pressure and serum ApoE levels [12].”
    • Also stated in: § Background · hedged
      “A recent study showed that patients with ApoE mutations in the LDLR binding area may have relatively high blood pressure and serum ApoE [12], suggesting phenotype differences among various ApoE mutations.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [12] Yang M, Weng Q, Pan X, Hussain HMJ, Yu S, Xu J, et al. Clinical and genetic analysis of lipoprotein glomerulopathy patients caused by APOE mutations. Mol Genet Genomic Med. 2020; e1281. source

      The Results (Literature review; page unavailable) report higher serum apoE in LPG patients with LDL receptor binding-region mutations than in patients with mutations elsewhere. They also report higher blood pressure for LPG patients overall than for controls, but do not establish higher blood pressure specifically for the binding-region subgroup. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    ApoE Kyoto and ApoE Sendai both have significantly reduced helical content and are thermodynamically destabilized and prone to aggregation.

    “ApoE Kyoto and ApoE Sendai both have significantly reduced helical content and are thermodynamically destabilized and prone to aggregation [13].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [13] Katsarou M, Stratikos E, Chroni A. Thermodynamic destabilization and aggregation propensity as the mechanism behind the association of apoE3 mutants and lipoprotein glomerulopathy. J Lipid Res. 2018;59(12):2339–48. source

  • May combine two claims.

    Findingown data

    There were no significant changes in serum triglyceride and urinary albumin-creatinine ratio among the five groups.

    “There were no significant changes in serum triglyceride and urinary albumin–creatinine ratio among the five groups.”
    • Also stated in: § Plasma total cholesterol and triglyceride and urine albumin–creatinine ratio detection · hedged
      “the triglyceride and urine ACR levels had no apparent changes in the five groups during the observation period”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Serum total cholesterol decreased by 63%, 65%, and 73% in the AD-ApoE Kyoto, AD-ApoE Sendai, and AD-ApoE3 groups, respectively.

    “The serum total cholesterol decreased by 63%, 65%, and 73% in the AD-ApoE Kyoto, AD-ApoE Sendai and AD-ApoE3 groups, respectively.”
    • Also stated in: § Plasma total cholesterol and triglyceride and urine albumin–creatinine ratio detection · plain
      “The relative reduction in total cholesterol level was 63%, 65%, and 73% in the AD-ApoE Kyoto, AD-ApoE Sendai, and AD-ApoE3 groups, respectively.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingnone given

    Adenovirus-mediated expression of ApoE variants lasted only 7-10 days and then decreased, unlike the sustained expression of ApoE mutants in human LPG.

    “adenovirus-mediated expression of ApoE variants can only last for 7–10 days and can immediately decrease thereafter; this was not consistent with the sustained expression of ApoE mutants in human LPG.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    LPG-like renal lesions were observed in three mice of the AD-ApoE Kyoto group and in one mouse of the AD-ApoE Sendai group.

    “LPG-like renal lesions were observed in three mice of the AD-ApoE Kyoto group and in one mouse of the AD-ApoE Sendai group.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    After virus injection, plasma human ApoE reached maximum levels at 4-6 days in the AD-ApoE Kyoto and AD-ApoE Sendai groups (17.4 ± 3.1 μg/mL vs 22.2 ± 4.5 μg/mL, respectively) and at 2 days in the AD-ApoE3 group (38.4 μg/mL).

    “After virus injection, plasma human ApoE was detected and rapidly reached the maximum level at 4–6 days in the AD-ApoE Kyoto and AD-ApoE Sendai groups (17.4 ± 3.1 µg/mL vs.: 22.2 ± 4.5 µg/mL, respectively) and at 2 days in the AD-ApoE3 group (38.4 µg/mL).”
    • Also stated in: § Quantification of human ApoE in the plasma of ApoE (−/−) mice · plain
      “In the AD-ApoE Sendai and AD-ApoE Kyoto groups, human ApoE was detected on the 2nd day; reached the peak levels of 22.2 µg/mL and 17.4 µg/mL, respectively, after 4–6 days; and declined to the baseline level on the 10th day.”
    • Also stated in: § Quantification of human ApoE in the plasma of ApoE (−/−) mice · plain
      “In the AD-ApoE3 group, the expression of plasma human ApoE rapidly reached a peak of 38.4 µg/mL on the 2nd day after virus injection and declined to a low level on the 10th day.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The Oil-red O-positive glomerular area was 9.2% in the AD-ApoE Kyoto group and tended to be higher than in the AD-ApoE Sendai (3.9%), AD-ApoE3 (4.8%), AD-eGFP (2.9%), and ApoE (−/−) (3.6%) groups.

    “The Oil-red O-positive glomerular area tended to be higher in the AD-ApoE Kyoto group (9.2%) than in the AD-ApoE Sendai (3.9%), AD-ApoE3 (4.8%), AD-eGFP (2.9%), and ApoE (−/−) (3.6%) groups.”
    • Also stated in: § Histologic manifestation of renal lesions · hedged
      “The Oil-red O-positive glomerular area in AD-ApoE Kyoto group was 9.2% and tended to be higher, compared with that in the other groups [3.9% in AD-ApoE Sendai, 4.8% in AD-apoE3, 2.9% in AD-eGFP, and 3.6%, in ApoE (−/−) groups].”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    ApoE Sendai is located in the LDLR binding area, and its affinity for LDLR is decreased.

    “ApoE Sendai is located in the LDLR binding area, and the affinity of ApoE Sendai for LDLR was decreased [10].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] Ishigaki Y, Oikawa S, Suzuki T, Usui S, Magoori K, Kim DH, et al. Virus-mediated transduction of apolipoprotein E (ApoE)-sendai develops lipoprotein glomerulopathy in ApoE-deficient mice. J Biol Chem. 2000;275(40):31269–73. source

  • May combine two claims.

    Premisecitation

    Triglyceride-rich lipoprotein containing ApoE Kyoto has increased affinity for endothelial cells, which may manifest as local adhesion.

    “triglyceride-rich lipoprotein containing ApoE Kyoto had been shown to have increased affinity for endothelial cells, and this may be manifested as local adhesion [14].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [14] Murano T, Matsumura R, Misawa Y, Ozaki H, Miyashita Y, Yoshida S, et al. Interaction of endothelial cells and triglyceride-rich lipoproteins with apolipoprotein E (Arg25[rarr ]Cys) from a patient with lipoprotein glomerulopathy. Metabolism. 2002;51(2):201–5. source

  • May combine two claims.

    Premisecitation

    ApoE Kyoto has reduced affinity for LDLR and is located outside the LDLR binding area.

    “Although ApoE Kyoto has reduced affinity for LDLR, it is located outside the LDLR binding area.”
    • Also stated in: § Background · plain
      “Matsunaga et al. showed that the binding ability of recombinant apoE3 Kyoto to LDLR was reduced to 10%, compared with that of recombinant apoE3, in vitro [11].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [11] Matsunaga A, Sasaki J, Komatsu T, Kanatsu K, Tsuji E, Moriyama K, et al. A novel apolipoprotein E mutation, E2 (Arg25Cys), in lipoprotein glomerulopathy. Kidney Int. 1999;56(2):421–7. source

  • May combine two claims.

    Interpretationown data

    ApoE Kyoto may induce LPG while protecting against atherosclerosis.

    “ApoE Kyoto may induce LPG while protecting against atherosclerosis.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    ApoE Kyoto mutation is pathogenic in lipoprotein glomerulopathy, as validated in an ApoE-deficient mouse model.

    “We validated the pathogenicity of ApoE Kyoto in LPG using an animal study.”
    • Also stated in: § Conclusions · boosted
      “In this animal study, we first established an ApoE Kyoto mutation murine model and confirmed its pathogenic role in LPG.”
    • Also stated in: § Discussion · boosted
      “All of the above supported the pathogenicity of ApoE Kyoto in LPG.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Yamamoto et al. proved the pathogenicity of ApoE Sendai by developing LPG in ApoE-deficient mice using virus-mediated transduction of ApoE Sendai.

    “Yamamoto et al. proved the pathogenicity of ApoE Sendai by developing LPG in ApoE-deficient mice using virus-mediated transduction of ApoE Sendai [10].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] Ishigaki Y, Oikawa S, Suzuki T, Usui S, Magoori K, Kim DH, et al. Virus-mediated transduction of apolipoprotein E (ApoE)-sendai develops lipoprotein glomerulopathy in ApoE-deficient mice. J Biol Chem. 2000;275(40):31269–73. source

  • May combine two claims.

    Premisecitation

    In the study by Yamamoto, expression of ApoE Sendai resulted in insufficient normalization of hypercholesterolemia in ApoE-deficient mice and induced high plasma levels of triglyceride.

    “In the study by Yamamoto, the expression of ApoE Sendai resulted in insufficient normalization of hypercholesterolemia in ApoE-deficient mice and induced high plasma levels of triglyceride [10].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Ishigaki Y, Oikawa S, Suzuki T, Usui S, Magoori K, Kim DH, et al. Virus-mediated transduction of apolipoprotein E (ApoE)-sendai develops lipoprotein glomerulopathy in ApoE-deficient mice. J Biol Chem. 2000;275(40):31269–73. source

  • Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).

    Study design and conductreasoning

    It is especially difficult to compare the two pathogenic variants of apoE in this study.

    “It is especially difficult to compare the two pathogenic variants of apoE.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    Kanamaru et al. presented that LPG-like lesions could be observed in FcRγ-deficient mice.

    “Kanamaru et al. [17] presented that LPG-like lesions could be observed in FcRγ-deficient mice.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [17] Kanamaru Y, Nakao A, Shirato I, Okumura K, Ogawa H, Tomino Y, et al. Chronic graft-versus-host autoimmune disease in Fc receptor gamma chain-deficient mice results in lipoprotein glomerulopathy. J Am Soc Nephrol. 2002;13(6):1527–33. source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Genotype was determined before the experiment.

    “genotype was determined before experiment.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Twenty-seven weight- and age-matched male ApoE−/− mice were randomly divided into five groups.

    “Twenty-seven weight- and age-matched (3 months of age) male ApoE (−/−) mice were randomly divided into five groups”
    Quote in the paperNot a substantial claim
19 of 19

  • The paper relies on this without support.

    ApoE Kyoto is the most common ApoE mutation in LPG.

    “ApoE Kyoto has been the most common mutation in LPG.”

  • The paper relies on this without support.

    The similarity of ApoE between human and mouse is about 71%.

    “The similarity of ApoE between human and mouse is about 71%.”

  • The paper relies on this without support.

    In human LPG, foam-like macrophages in the glomeruli are rare.

    “Usually, in human LPG, foam-like macrophages in the glomeruli are rare.”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In animal models, APOE Sendai (Arg145Pro) and APOE Kyoto (Arg25Cys) variants have been expressed in APOE-deficient mice, with LPG-like renal pathology having been observed in each.

    “In animal models, APOE Sendai (Arg145Pro) and APOE Kyoto (Arg25Cys) variants have been expressed in APOE-deficient mice, with LPG-like renal pathology having been observed in each95, 96).”

    From Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features (2025) · cites this paper as [96]

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Wu H, Yang Y, Hu Z. The novel apolipoprotein E mutation ApoE Chengdu (c.518TC, p.L173P) in a Chinese patient with lipoprotein glomerulopathy. J Atheroscler Thromb. 2018;25:733–40. · DOI · Paper page

Cited by

Sorted by citations

Related

Authors
Wu, H., Yang, J., Liu, Y.-Q., Lei, S., Yang, M., Yang, Z., Yang, Y., & Hu, Z.
Affiliations
Sichuan University (CN)
Corresponding author
Hu, Zhangxue
ORCID
Venue
Journal of Translational Medicine
Publisher
Springer Science and Business Media LLC
Published
2021-03-04
Volume
19
Issue
1
Pages
97-97
ISSN
1479-5876 (ISSN-L)
DOI
10.1186/s12967-021-02765-x
PMC
PMC7934380
OpenAlex
W3135865831
Cited by
10
References
21
Citations by year
2025: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 1
FWCI
1.37
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Translational Medicine (publishedVersion, cc-by)
  • Research Square (acceptedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (81470916)
  • Chengdu Municipal Bureau of Science and Technology (0040205301D74)
  • Sichuan Province Key Technology R&D Program (18ZDYF2112)
Topics
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords
lipoprotein glomerulopathy, ApoE-deficient mice, adenoviral gene transfer, atherosclerosis, serum cholesterol, APOE3, albuminuria, triglycerides
MeSH terms
Mice, Knockout, ApoE, Animals, Apolipoproteins E, Kidney Diseases, Kidney Glomerulus, Male, Mutation, Mice

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