Cited by 254

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Genome-wide identification of microRNAs regulating cholesterol and triglyceride homeostasis

Wagschal, Alexandre, Najafi-Shoushtari, S Hani, Wang, Lifeng, Goedeke, Leigh, Sinha, Sumita, deLemos, Andrew S, Black, Josh C, Ramírez, Cristina M, Li, Yingxia, Tewhey, Ryan, Hatoum, Ida, Shah, Naisha, Lu, Yong, Kristo, Fjoralba, Psychogios, Nikolaos, Vrbanac, Vladimir, Lu, Yi-Chien, Hla, Timothy, de Cabo, Rafael, Tsang, John S, Schadt, Eric, Sabeti, Pardis C, Kathiresan, Sekar, Cohen, David E, Whetstine, Johnathan, Chung, Raymond T, Fernández-Hernando, Carlos, Kaplan, Lee M, Bernards, Andre, Gerszten, Robert E, Näär, Anders M·2015·Nature Medicine

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nm.3980

Cites

9 of 9 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Numerous miRNAs directly bind LDLR mRNA 3′UTR and decrease its expression, including miR-27a, miR-27b, miR-128-1, miR-128-3p, miR-130b, miR-148a, miR-184a, miR-185, and miR-301b.

    “Numerous miRNAs have been shown to directly bind LDLR mRNA 3' UTR and decrease its expression (Fig. 2), including miR-27a, miR-27b, miR-128-1, miR-128-3p, miR-130b, miR-148a, miR-184a, miR-185, and miR-301b [43][44][45][46][47][48].”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [46]

    The Results section (‘MicroRNA regulation of lipid-related genes and cholesterol and lipoprotein trafficking’; page unavailable) shows that miR-128-1, miR-148a, miR-130b, and miR-301b repress LDLR through its 3′ UTR: mutating their predicted target sites abolished the repression. Our copy does not establish that the other listed miRNAs—miR-27a, miR-27b, miR-128-3p, miR-184a, and miR-185—do so. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • miR-27a, miR-27b, miR-128-1, miR-128-3p, miR-130b, miR-148a, miR-184a, miR-185, and miR-301b inhibit expression of the LDLR, decreasing LDLR.

    “miR-27a, miR-27b, miR-128-1, miR-128-3p, miR-130b, miR-148a, miR-184a, miR-185, miR-301b Inhibit expression of the LDLR ↓ [43-48]”

    From The low-density lipoprotein receptor: Emerging post-transcriptional regulatory mechanisms (2025) · cites this paper as [46]

    The Results section on microRNA regulation of lipid-related genes reports that miR-128-1, miR-130b, miR-148a, and miR-301b decreased LDLR levels in HepG2 cells. It does not establish the claimed LDLR inhibition for the other five listed miRNAs: miR-27a, miR-27b, miR-128-3p, miR-184a, and miR-185. Page numbers are unavailable in our copy. (LLM, conf=0.90)

    Experimental — accuracy not yet measured
  • miR-128-1 is located within intron 18 of R3HDM1, and its expression is dependent on expression of its host gene.

    “miR-128-1 is located within intron 18 of R3HDM1 and its expression is dependent on the expression of its host gene51.”

    From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [51]

    The Results section, “MicroRNAs are linked to SNPs associated with abnormal blood lipids” (page unavailable), places miR-128-1 in intron 18 of R3HDM1. It says the two appear extensively co-expressed, suggesting a shared primary transcript, but does not establish that miR-128-1 expression depends on host-gene expression. (LLM, conf=0.90)

    Experimental — accuracy not yet measured
  • Another GWAS identified miR-130b and miR-301b, miR-128-1, and miR-148a as highly associated with metabolic control in cardiometabolic disorders.

    “Another GWAS identified miR-130b and miR-301b, two related miRNAs derived from the same seed sequence, miR-128-1, as well as miR-148a, as being highly associated with metabolic control in cardiometabolic disorders51.”
  • miR-148a is primarily expressed in the liver, and its expression is induced in mice and rhesus macaques fed a high fat diet.

    “miR-148a is primarily expressed in the liver and expression is induced in mice and rhesus macaques fed a high fat diet51.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 40

  1. Quiat, D. & Olson, E.N. MicroRNAs in cardiovascular disease: from pathogenesis to prevention and treatment. J. Clin. Invest. 123, 11–18 (2013). · DOI
  2. Rottiers, V. & Naar, A.M. MicroRNAs in metabolism and metabolic disorders. Nat. Rev. Mol. Cell Biol. 13, 239–250 (2012). · DOI · Paper page
  3. Marquart, T.J., Allen, R.M., Ory, D.S. & Baldan, A. miR-33 links SREBP-2 induction to repression of sterol transporters. Proc. Natl. Acad. Sci. USA 107, 12228–12232 (2010). · DOI · Paper page
  4. Horie, T. et al. MicroRNA-33 encoded by an intron of sterol regulatory element-binding protein 2 (Srebp2) regulates HDL in vivo. Proc. Natl. Acad. Sci. USA 107, 17321–17326 (2010). · DOI · Paper page
  5. Rayner, K.J. et al. Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides. Nature 478, 404–407 (2011). · DOI · Paper page
  6. Goedeke, L., Aranda, J.F. & Fernandez-Hernando, C. microRNA regulation of lipoprotein metabolism. Curr. Opin. Lipidol. 25, 282–288 (2014). · DOI
  7. Willer, C.J. et al. Discovery and refinement of loci associated with lipid levels. Nat. Genet. 45, 1274–1283 (2013). · DOI
  8. Merino, D.M., Ma, D.W. & Mutch, D.M. Genetic variation in lipid desaturases and its impact on the development of human disease. Lipids Health Dis. 9, 63 (2010). · DOI
  9. Charles, M.A. & Kane, J.P. New molecular insights into CETP structure and function: a review. J. Lipid Res. 53, 1451–1458 (2012). · DOI
  10. Lewis, B.P., Burge, C.B. & Bartel, D.P. Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets. Cell 120, 15–20 (2005). · DOI · Paper page
  11. Ishibashi, S. et al. Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery. J. Clin. Invest. 92, 883–893 (1993). · DOI · Paper page
  12. Brown, M.S. & Goldstein, J.L. How LDL receptors influence cholesterol and atherosclerosis. Sci. Am. 251, 58–66 (1984). · DOI · Paper page
  13. Tall, A.R., Yvan-Charvet, L., Terasaka, N., Pagler, T. & Wang, N. HDL, ABC transporters, and cholesterol efflux: implications for the treatment of atherosclerosis. Cell Metab. 7, 365–375 (2008). · DOI · Paper page
  14. Navab, M., Reddy, S.T., Van Lenten, B.J. & Fogelman, A.M. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nat. Rev. Cardiol. 8, 222–232 (2011). · DOI
  15. Duffy, D. & Rader, D.J. Update on strategies to increase HDL quantity and function. Nat. Rev. Cardiol. 6, 455–463 (2009). · DOI
  16. Sparks, J.D., Sparks, C.E. & Adeli, K. Selective hepatic insulin resistance, VLDL overproduction, and hypertriglyceridemia. Arterioscler. Thromb. Vasc. Biol. 32, 2104–2112 (2012). · DOI
  17. Stein, S. & Matter, C.M. Protective roles of SIRT1 in atherosclerosis. Cell Cycle 10, 640–647 (2011). · DOI · Paper page
  18. Yoon, Y.S., Seo, W.Y., Lee, M.W., Kim, S.T. & Koo, S.H. Salt-inducible kinase regulates hepatic lipogenesis by controlling SREBP-1c phosphorylation. J. Biol. Chem. 284, 10446–10452 (2009). · DOI
  19. Hardie, D.G. Organismal carbohydrate and lipid homeostasis. Cold Spring Harb. Perspect. Biol. 4 (2012). · DOI
  20. Bonnefont, J.P. et al. Carnitine palmitoyltransferases 1 and 2: biochemical, molecular and medical aspects. Mol. Aspects Med. 25, 495–520 (2004). · DOI · Paper page
  21. Goldstein, J.L., DeBose-Boyd, R.A. & Brown, M.S. Protein sensors for membrane sterols. Cell 124, 35–46 (2006). · DOI · Paper page
  22. Goldstein, J.L. & Brown, M.S. The LDL receptor. Arterioscler. Thromb. Vasc. Biol. 29, 431–438 (2009). · DOI · Paper page
  23. Soutar, A.K. & Naoumova, R.P. Mechanisms of disease: genetic causes of familial hypercholesterolemia. Nat. Clin. Pract. Cardiovasc. Med. 4, 214–225 (2007). · DOI · Paper page
  24. Lu, Y.C. et al. ELAVL1 modulates transcriptome-wide miRNA binding in murine macrophages. Cell Rep. 9, 2330–2343 (2014). · DOI
  25. Zhang, S.H., Reddick, R.L., Piedrahita, J.A. & Maeda, N. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258, 468–471 (1992). · DOI · Paper page
  26. Hatoum, I.J. et al. Melanocortin-4 receptor signaling is required for weight loss after gastric bypass surgery. J. Clin. Endocrinol. Metab. 97, E1023–E1031 (2012). · DOI
  27. Greenawalt, D.M. et al. A survey of the genetics of stomach, liver, and adipose gene expression from a morbidly obese cohort. Genome Res. 21, 1008–1016 (2011). · DOI
  28. Hatoum, I.J. et al. Weight loss after gastric bypass is associated with a variant at 15q26.1. Am. J. Hum. Genet. 92, 827–834 (2013). · DOI
  29. Raymond, C.K., Roberts, B.S., Garrett-Engele, P., Lim, L.P. & Johnson, J.M. Simple, quantitative primer-extension PCR assay for direct monitoring of microRNAs and short-interfering RNAs. RNA 11, 1737–1744 (2005). · DOI
  30. Liu, E.Y., Li, M., Wang, W. & Li, Y. MaCH-admix: genotype imputation for admixed populations. Genet. Epidemiol. 37, 25–37 (2013). · DOI
  31. Shabalin, A.A. Matrix eQTL: ultra fast eQTL analysis via large matrix operations. Bioinformatics 28, 1353–1358 (2012). · DOI · Paper page
  32. Weischenfeldt, J. & Porse, B. Bone marrow-derived macrophages (BMM): isolation and applications. CSH Protoc 2008 doi:10.1101/pdb.prot5080 (2010). · DOI
  33. Hafner, M. et al. Identification of microRNAs and other small regulatory RNAs using cDNA library sequencing. Methods 44, 3–12 (2008). · DOI
  34. Hafner, M. et al. Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP. Cell 141, 129–141 (2010). · DOI · Paper page
  35. Corcoran, D.L. et al. PARalyzer: definition of RNA binding sites from PAR-CLIP short-read sequence data. Genome Biol. 12, R79 (2011). · DOI
  36. Mattison, J.A. et al. Resveratrol prevents high fat/sucrose diet-induced central arterial wall inflammation and stiffening in nonhuman primates. Cell Metab. 20, 183–190 (2014). · DOI
  37. Rayner, K.J. et al. MiR-33 contributes to the regulation of cholesterol homeostasis. Science 328, 1570–1573 (2010). · DOI · Paper page
  38. Lillie, R.D. & Fulmer, H.M. Histopathologic Technique and Practical Histochemistry. (McGraw-Hill, 1976).
  39. Ljungberg, O. & Tibblin, S. Peroperative fat staining of frozen sections in primary hyperparathyroidism. Am. J. Pathol. 95, 633–641 (1979).
  40. Galabova, G. et al. Peptide-based anti-PCSK9 vaccines - an approach for long-term LDLc management. PLoS ONE 9, e114469 (2014). · DOI

Cited by

Sorted by citations

Metadata

Authors
Wagschal, A., Najafi-Shoushtari, S. H., Wang, L., Goedeke, L., Sinha, S., deLemos, A. S., Black, J. C., Ramírez, C. M., Li, Y., Tewhey, R., Hatoum, I., Shah, N., Lu, Y., Kristo, F., Psychogios, N., Vrbanac, V., Lu, Y.-C., Hla, T., de Cabo, R., Tsang, J. S., Schadt, E., Sabeti, P. C., Kathiresan, S., Cohen, D. E., Whetstine, J., Chung, R. T., Fernández-Hernando, C., Kaplan, L. M., Bernards, A., Gerszten, R. E., & Näär, A. M.
Venue
Nature Medicine
Published
2015-10-26
Volume
21
Issue
11
Pages
1290-1297
ISSN
  • 1078-8956
  • 1546-170X
Cited by
254
References
9
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review