Cited by 284Mitochondrial Function and PathologyCell death mechanisms and regulationAutophagy in Disease and Therapy

Humanin: a harbinger of mitochondrial-derived peptides

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Lee, Changhan, Yen, Kelvin, Cohen, Pinchas·2013·Trends in Endocrinology & Metabolism

Abstract

Mitochondria have been largely considered as 'end-function' organelles, servicing the cell by producing energy and regulating cell death in response to complex signals. Being cellular entities with vital roles, mitochondria communicate back to the cell and actively engage in determining major cellular policies. These signals, collectively referred to as retrograde signals, are encoded in the nuclear genome or are secondary products of mitochondrial metabolism. Here, we discuss humanin, the first small peptide of a putative set of mitochondrial-derived peptides (MDPs), which exhibits strong cytoprotective actions against various stress and disease models. The study of humanin and other mitochondrial-derived retrograde signal peptides will aid in the identification of genes and peptides with therapeutic and diagnostic potential in treating human diseases.

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Crossref · 10.1016/j.tem.2013.01.005

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  • HN fulfills features of a mitochondrial retrograde response molecule.

    “The previously discovered 24-aa peptide encoded by mitochondrial DNA indicated as HN also fulfilled the features of a mitochondrial retrograde response molecule (39).”

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Authors
Lee, C., Yen, K., & Cohen, P.
Affiliations
University of Southern California (US)
Corresponding author
Cohen, Pinchas
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2013-05
Volume
24
Issue
5
Pages
222-228
ISSN
1043-2760 (ISSN-L)
OpenAlex
W2111941596
Cited by
284
References
59
Citations by year
2026: 19 · 2025: 13 · 2024: 18 · 2023: 30 · 2022: 19 · 2021: 27 · 2020: 32 · 2019: 27 · 2018: 26 · 2017: 17 · 2016: 20 · 2015: 14 · 2014: 16 · 2013: 6
FWCI
1.76
Type
journal article
Language
en
Open access
Locations
  • Trends in Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (7r01ag034430-05)
  • National Institute on Aging (# R01AG034430)
  • National Institute of General Medical Sciences (R01GM090311)
  • National Institute of Environmental Health Sciences (R01ES020812)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
humanin, mitochondrial peptides, retrograde signaling, mitochondria, cytoprotection, mitochondrial stress, cell death regulation, energy metabolism, peptide therapeutics
MeSH terms
Animals, Cell Nucleus, DNA, Mitochondrial, Humans, Mitochondria, Models, Biological, Signal Transduction, Retroelements, Intracellular Signaling Peptides and Proteins

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