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Hamster — Atherosclerosis (hereditary; OMIA-verified species predisposition)

companion_species_health_omia_5017_hamster

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--- license: permission_granted topic_id: companion_species_health_omia_5017_hamster category: companion-species-health title: "Hamster — Atherosclerosis (hereditary; OMIA-verified species predisposition)" lang: en source: "OMIA (Online Mendelian Inheritance in Animals, University of Sydney) species-specific hereditary-disorder record, saved verbatim to source_file; C1 substring-verified. Pulled 2026-08-24 from local OMIA database dump." source_file: pdf-raw/species-health/hamster_omia_5017_5017.txt date_parsed: 2026-08-24 tokens_estimated: 182 verification: method: substring_match claims: 4 passed: 4 date: 2026-08-24 recovered: false path: companion-species-health/companion_species_health_omia_5017_hamster/01_companion_species_health_omia_5017_hamster.md source_document: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" citation: authority: "OMIA — Online Mendelian Inheritance in Animals (University of Sydney)" title: "Hamster — Atherosclerosis (hereditary; OMIA-verified species predisposition)" url: "https://omia.org/OMIA000080/10036/" retrieved: "2026-08-24" ref: "OMIA species-specific hereditary-disorder records (omia.org), derived from local OMIA database dump; dataset: https://doi.org/10.25910/2AMR-PV70" doc_type: "academic animal-genetics database (species-specific disorder entries)" needs_review: false

verification_derived: method: derived_from_dataset source: "OMIA database dump (omia.xml, local); fields Gene/Variant/Article/OMIM" note: "Structured fields (gene, variant rsID/protein change, PubMed/DOI references, OMIM cross-link) extracted from OMIA dump and presented with first-hand values; not verbatim prose." verification_derived: method: derived_from_dataset source: "OMIA database dump (omia.xml, local); fields Gene/Variant/Article/OMIM" note: "Structured fields (gene, variant rsID/protein change, PubMed/DOI references, OMIM cross-link) extracted from OMIA dump and presented with first-hand values; not verbatim prose." verification_derived: method: derived_from_dataset source: "OMIA database dump (omia.xml, local); fields Gene/Variant/Article/OMIM" note: "Structured fields (gene, variant rsID/protein change, PubMed/DOI references, OMIM cross-link) extracted from OMIA dump and presented with first-hand values; not verbatim prose."---

Hamster — Atherosclerosis (hereditary; OMIA-verified species predisposition)

Source: first-hand OMIA (University of Sydney) species-specific hereditary-disorder record, saved verbatim to source_file; every claim below is a C1 byte-substring of it.

Claims

  • Species: Mesocricetus auratus / Phodopus spp. (hamster)
  • Disorder:
  • Summary: Hamsters have been used as models for dyslipidemia and atherosclerosis for many decades. Xian et al. (2022) summarise their research relating to several CRISPR/Cas9 genetically engineered hamster models for dyslipidemia, created by targeting low density lipoprotein receptor (LDLR) (Wu et al., 2019), lecithin cholesterol acyl transferase (LCAT) (Dong et al., 2018), ApoC2 (Gao et al., 2020), ApoC3 (Guo et al., 2020), and adenosine triphosphate-binding cassette transporter A1 (ABCA1) (Wei et al., 2019) genes. This entry includes references to studies involving gene edited organisms (GMO).
  • Defect: yes

Evidence (references)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • 2022. Genetically engineered hamster models of dyslipidemia and atherosclerosis. Methods Mol Biol — PubMed:PMID35237980 | DOI:10.1007/978-1-0716-1924-7_26 — OMIA Phene_Article / Article
  • 1987. The hyperlipidemic hamster as a model of experimental atherosclerosis. Atherosclerosis — PubMed:PMID3689479 | DOI:10.1016/0021-9150(87)90106-7 — OMIA Phene_Article / Article
  • 1950. Experimental cholesterol arteriosclerosis. II. Changes produced in golden hamsters and in guinea pigs. Am Heart J — PubMed:PMID14770982 | DOI:10.1016/0002-8703(50)90323-1 — OMIA Phene_Article / Article
  • 2019. Heterozygous Ldlr-deficient hamster as a model to evaluate the efficacy of PCSK9 antibody in hyperlipidemia and atherosclerosis. Int J Mol Sci — PubMed:PMID31779098 | DOI:10.3390/ijms20235936 — OMIA Phene_Article / Article
  • 2018. Loss of LCAT activity in the golden Syrian hamster elicits pro-atherogenic dyslipidemia and enhanced atherosclerosis. Metabolism — PubMed:PMID29526535 | DOI:10.1016/j.metabol.2018.03.003 — OMIA Phene_Article / Article
  • 2020. ApoC2 deficiency elicits severe hypertriglyceridemia and spontaneous atherosclerosis: A rodent model rescued from neonatal death. Metabolism — PubMed:PMID32562799 | DOI:10.1016/j.metabol.2020.154296 — OMIA Phene_Article / Article
  • 2020. Inactivation of ApoC3 by CRISPR/Cas9 protects against atherosclerosis in hamsters. Circ Res — PubMed:PMID32951534 | DOI:10.1161/CIRCRESAHA.120.317686 — OMIA Phene_Article / Article
  • 2019. Impact of cholesterol on ischemic stroke in different human-like hamster models: A new animal model for ischemic stroke study. Cells — PubMed:PMID31487778 | DOI:10.3390/cells8091028 — OMIA Phene_Article / Article
  • 2023. Depleting LCAT aggravates atherosclerosis in LDLR-deficient hamster with reduced LDL-Cholesterol level. J Adv Res — PubMed:PMID37923248 | DOI:10.1016/j.jare.2023.10.016 — OMIA Phene_Article / Article
  • 2025. ApoL1 risk allele accelerates high-fat diet-induced atherosclerosis in LDLR-/- hamsters. Genes Dis — PubMed:PMID39669548 | DOI:10.1016/j.gendis.2024.101379 — OMIA Phene_Article / Article
  • 2025. Loss of LCAT function aggravates metabolic associated steatohepatitis (MASH) in golden Syrian hamster. Clin Sci (Lond) — PubMed:PMID41195480 | DOI:10.1042/CS20257764 — OMIA Phene_Article / Article
  • 2026. AAV gene therapy for homozygous familial hypercholesterolemia: a phase 1 trial. Nat Med — PubMed:PMID42243546 | DOI:10.1038/s41591-026-04441-3 — OMIA Phene_Article / Article

Comparative medicine (human OMIM)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • OMIM:108725 (type: trait) — OMIA Group_OMIM (via OMIA_ID)

Evidence (references)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • 2022. Genetically engineered hamster models of dyslipidemia and atherosclerosis. Methods Mol Biol — PubMed:PMID35237980 | DOI:10.1007/978-1-0716-1924-7_26 — OMIA Phene_Article / Article
  • 1987. The hyperlipidemic hamster as a model of experimental atherosclerosis. Atherosclerosis — PubMed:PMID3689479 | DOI:10.1016/0021-9150(87)90106-7 — OMIA Phene_Article / Article
  • 1950. Experimental cholesterol arteriosclerosis. II. Changes produced in golden hamsters and in guinea pigs. Am Heart J — PubMed:PMID14770982 | DOI:10.1016/0002-8703(50)90323-1 — OMIA Phene_Article / Article
  • 2019. Heterozygous Ldlr-deficient hamster as a model to evaluate the efficacy of PCSK9 antibody in hyperlipidemia and atherosclerosis. Int J Mol Sci — PubMed:PMID31779098 | DOI:10.3390/ijms20235936 — OMIA Phene_Article / Article
  • 2018. Loss of LCAT activity in the golden Syrian hamster elicits pro-atherogenic dyslipidemia and enhanced atherosclerosis. Metabolism — PubMed:PMID29526535 | DOI:10.1016/j.metabol.2018.03.003 — OMIA Phene_Article / Article
  • 2020. ApoC2 deficiency elicits severe hypertriglyceridemia and spontaneous atherosclerosis: A rodent model rescued from neonatal death. Metabolism — PubMed:PMID32562799 | DOI:10.1016/j.metabol.2020.154296 — OMIA Phene_Article / Article
  • 2020. Inactivation of ApoC3 by CRISPR/Cas9 protects against atherosclerosis in hamsters. Circ Res — PubMed:PMID32951534 | DOI:10.1161/CIRCRESAHA.120.317686 — OMIA Phene_Article / Article
  • 2019. Impact of cholesterol on ischemic stroke in different human-like hamster models: A new animal model for ischemic stroke study. Cells — PubMed:PMID31487778 | DOI:10.3390/cells8091028 — OMIA Phene_Article / Article
  • 2023. Depleting LCAT aggravates atherosclerosis in LDLR-deficient hamster with reduced LDL-Cholesterol level. J Adv Res — PubMed:PMID37923248 | DOI:10.1016/j.jare.2023.10.016 — OMIA Phene_Article / Article
  • 2025. ApoL1 risk allele accelerates high-fat diet-induced atherosclerosis in LDLR-/- hamsters. Genes Dis — PubMed:PMID39669548 | DOI:10.1016/j.gendis.2024.101379 — OMIA Phene_Article / Article
  • 2025. Loss of LCAT function aggravates metabolic associated steatohepatitis (MASH) in golden Syrian hamster. Clin Sci (Lond) — PubMed:PMID41195480 | DOI:10.1042/CS20257764 — OMIA Phene_Article / Article
  • 2026. AAV gene therapy for homozygous familial hypercholesterolemia: a phase 1 trial. Nat Med — PubMed:PMID42243546 | DOI:10.1038/s41591-026-04441-3 — OMIA Phene_Article / Article

Comparative medicine (human OMIM)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • OMIM:108725 (type: trait) — OMIA Group_OMIM (via OMIA_ID)

Evidence (references)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • 2022. Genetically engineered hamster models of dyslipidemia and atherosclerosis. Methods Mol Biol — PubMed:PMID35237980 | DOI:10.1007/978-1-0716-1924-7_26 — OMIA Phene_Article / Article
  • 1987. The hyperlipidemic hamster as a model of experimental atherosclerosis. Atherosclerosis — PubMed:PMID3689479 | DOI:10.1016/0021-9150(87)90106-7 — OMIA Phene_Article / Article
  • 1950. Experimental cholesterol arteriosclerosis. II. Changes produced in golden hamsters and in guinea pigs. Am Heart J — PubMed:PMID14770982 | DOI:10.1016/0002-8703(50)90323-1 — OMIA Phene_Article / Article
  • 2019. Heterozygous Ldlr-deficient hamster as a model to evaluate the efficacy of PCSK9 antibody in hyperlipidemia and atherosclerosis. Int J Mol Sci — PubMed:PMID31779098 | DOI:10.3390/ijms20235936 — OMIA Phene_Article / Article
  • 2018. Loss of LCAT activity in the golden Syrian hamster elicits pro-atherogenic dyslipidemia and enhanced atherosclerosis. Metabolism — PubMed:PMID29526535 | DOI:10.1016/j.metabol.2018.03.003 — OMIA Phene_Article / Article
  • 2020. ApoC2 deficiency elicits severe hypertriglyceridemia and spontaneous atherosclerosis: A rodent model rescued from neonatal death. Metabolism — PubMed:PMID32562799 | DOI:10.1016/j.metabol.2020.154296 — OMIA Phene_Article / Article
  • 2020. Inactivation of ApoC3 by CRISPR/Cas9 protects against atherosclerosis in hamsters. Circ Res — PubMed:PMID32951534 | DOI:10.1161/CIRCRESAHA.120.317686 — OMIA Phene_Article / Article
  • 2019. Impact of cholesterol on ischemic stroke in different human-like hamster models: A new animal model for ischemic stroke study. Cells — PubMed:PMID31487778 | DOI:10.3390/cells8091028 — OMIA Phene_Article / Article
  • 2023. Depleting LCAT aggravates atherosclerosis in LDLR-deficient hamster with reduced LDL-Cholesterol level. J Adv Res — PubMed:PMID37923248 | DOI:10.1016/j.jare.2023.10.016 — OMIA Phene_Article / Article
  • 2025. ApoL1 risk allele accelerates high-fat diet-induced atherosclerosis in LDLR-/- hamsters. Genes Dis — PubMed:PMID39669548 | DOI:10.1016/j.gendis.2024.101379 — OMIA Phene_Article / Article
  • 2025. Loss of LCAT function aggravates metabolic associated steatohepatitis (MASH) in golden Syrian hamster. Clin Sci (Lond) — PubMed:PMID41195480 | DOI:10.1042/CS20257764 — OMIA Phene_Article / Article
  • 2026. AAV gene therapy for homozygous familial hypercholesterolemia: a phase 1 trial. Nat Med — PubMed:PMID42243546 | DOI:10.1038/s41591-026-04441-3 — OMIA Phene_Article / Article

Comparative medicine (human OMIM)

Derived from OMIA database dump (omia.xml, local); structured field, not verbatim prose. First-hand values below are verbatim substrings of the topic's pdf-raw/omia/<phene_id>.txt source file.

  • OMIM:108725 (type: trait) — OMIA Group_OMIM (via OMIA_ID)

Sources

Hamster — Atherosclerosis (hereditary; OMIA-verified species predisposition)
companion-species-healthPMID 35237980

Machine access

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