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Cited by 31Metabolism and Genetic DisordersLipid metabolism and biosynthesisAutophagy in Disease and Therapy

Peroxisomes and their central role in metabolic interaction networks in humans.

Open access
Wanders, Ronald J. A., Waterham, Hans R., Ferdinandusse, Sacha·2018·Subcellular Biochemistry
DOI 10.1007/978-981-13-2233-4_15
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Abstract

Peroxisomes catalyze a number of essential metabolic functions and impairments in any of these are usually associated with major clinical signs and symptoms. In contrast to mitochondria which are autonomous organelles that can catalyze the degradation of fatty acids, certain amino acids and other compounds all by themselves, peroxisomes are non-autonomous organelles which are highly dependent on the interaction with other organelles and compartments to fulfill their role in metabolism. This includes mitochondria, the endoplasmic reticulum, lysosomes, and the cytosol. In this paper we will discuss the central role of peroxisomes in different metabolic interaction networks in humans, including fatty acid oxidation, ether phospholipid biosynthesis, bile acid synthesis, fatty acid alpha-oxidation and glyoxylate metabolism.

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Crossref · 10.1007/978-981-13-2233-4_15

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  • Fatty acid chain length is governed by a balance between elongation and degradation, a process thought to be regulated at ER-peroxisome contact sites.

    “Fatty acid chain length is governed by a balance between elongation and degradation, a process thought to be regulated at ER–peroxisome contact sites (Wanders et al., 2018; Schrader et al., 2020).”

    From The neurological pathology of peroxisomal ACBD5 deficiency – lessons from patients and mouse models (2025) · cites this paper as Wanders et al., 2018

    The indexed passages labeled Abstract contain bibliographic information, not the chapter’s discussion. Searches for fatty-acid chain length, elongation and degradation, and ER–peroxisome contact sites returned no passage addressing the claim, so the available copy cannot verify it. (LLM, conf=0.76)

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  • Loss of ACBD5 can disrupt multiple pathways (e.g., ether lipid, bile acid, or DHA synthesis; balancing VLCFA elongation and breakdown) that rely on the interplay between these organelles.

    “Loss of ACBD5 can therefore disrupt multiple pathways (e.g., ether lipid-, bile acid, or DHA synthesis; balancing the equilibrium between VLCFA elongation and breakdown) that rely on the interplay between these organelles (Figure 3; Wanders et al., 2018).”

    From The neurological pathology of peroxisomal ACBD5 deficiency – lessons from patients and mouse models (2025) · cites this paper as Wanders et al., 2018

    The available copy contains the chapter title and bibliographic metadata, but no passage addressing ACBD5 or the proposed metabolic effects. Searches for ACBD5, the named pathways, and peroxisomal interactions returned no substantive chapter text, so the claim cannot be checked against this copy. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

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Authors
Wanders, R. J. A., Waterham, H. R., & Ferdinandusse, S.
Affiliations
Amsterdam UMC Location University of Amsterdam (NL)
Corresponding author
Wanders, Ronald J. A.
ORCID
Venue
Subcellular Biochemistry
Publisher
Springer Singapore
Published
2018
Volume
89
Pages
345-365
ISSN
0306-0225 (ISSN-L)
DOI
10.1007/978-981-13-2233-4_15
OpenAlex
W2898777544
Cited by
31
References
58
Citations by year
2026: 3 · 2025: 3 · 2024: 3 · 2023: 6 · 2022: 5 · 2021: 3 · 2020: 5 · 2019: 2 · 2018: 1
FWCI
11.52
Type
book chapter
Language
en
Open access
Licence
Locations
  • Sub-cellular biochemistry/Subcellular biochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion, other-oa)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
peroxisomes, fatty acid oxidation, bile acid synthesis, glyoxylate metabolism, peroxisomal disorders, mitochondria, endoplasmic reticulum, lysosomes
MeSH terms
Bile Acids and Salts, Fatty Acids, Glyoxylates, Humans, Oxidation-Reduction, Peroxisomes, Metabolic Networks and Pathways

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