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The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan

Yen, Kelvin, Mehta, Hemal H., Kim, Su-Jeong, Lue, YanHe, Hoang, James, Guerrero, Noel, Port, Jenna, Bi, Qiuli, Navarrete, Gerardo, Brandhorst, Sebastian, Lewis, Kaitlyn Noel, Wan, Junxiang, Swerdloff, Ronald, Mattison, Julie A., Buffenstein, Rochelle, Breton, Carrie V., Wang, Christina, Longo, Valter, Atzmon, Gil, Wallace, Douglas, Barzilai, Nir, Cohen, Pinchas·2020·Aging
DOI 10.18632/aging.103534PMC PMC7343442
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Figure 1 Humanin overexpression is sufficient to increase lifespan in C. elegans. HN overexpression significantly increased lifespan in worms (average lifespan of 19.0 days) compared to wild-type/N2 (average lifespan 17.7 days) (A). This increase in lifespan was dependent on daf-16 as daf-16(mu86) mutants did not have any increase in lifespan when crossed with the humanin-tg strain (average lifespan 15.5 days vs 16.1 days respectively) (p < 0.2) (B). Hn-tg worms also had a significant decrease in body length, body fat, and reproductive output (C–E). *indicates p<.05.
Figure 1 Humanin overexpression is sufficient to increase lifespan in C. elegans. HN overexpression significantly increased lifespan in worms (average lifespan of 19.0 days) compared to wild-type/N2 (average lifespan 17.7 days) (A). This increase in lifespan was dependent on daf-16 as daf-16(mu86) mutants did not have any increase in lifespan when crossed with the humanin-tg strain (average lifespan 15.5 days vs 16.1 days respectively) (p < 0.2) (B). Hn-tg worms also had a significant decrease in body length, body fat, and reproductive output (C–E). *indicates p<.05.CC BY · PubMed Central
Figure 2 HN-tg mice phenocopy the transgenic worms and are protected from toxic insult. Humanin transgenic mice have a significant decrease in body length by 12% at 28 days of age (n= 5 for control and n=3 for the hn-tg mice) (A). Body weight at the same age was also decreased by 10.4% (n=26 and n=16 for control and hn-tg mice respectively) (B), while litter size decreased by 46.5% (n=10 and n=15 for control and hn-tg mice respectively) (C). When administered cyclophosphamide, mice have a decreased lymphocyte count and transgenic mice are protected from this toxin (n=6 or 7 per group) (D). Similarly, when examining germ cell apoptosis organized by spermatogenic stages in the same cyclophosphamide treated mice, humanin transgenic mice are significantly protected from CP induced apoptosis (E). * indicates p<.05.
Figure 2 HN-tg mice phenocopy the transgenic worms and are protected from toxic insult. Humanin transgenic mice have a significant decrease in body length by 12% at 28 days of age (n= 5 for control and n=3 for the hn-tg mice) (A). Body weight at the same age was also decreased by 10.4% (n=26 and n=16 for control and hn-tg mice respectively) (B), while litter size decreased by 46.5% (n=10 and n=15 for control and hn-tg mice respectively) (C). When administered cyclophosphamide, mice have a decreased lymphocyte count and transgenic mice are protected from this toxin (n=6 or 7 per group) (D). Similarly, when examining germ cell apoptosis organized by spermatogenic stages in the same cyclophosphamide treated mice, humanin transgenic mice are significantly protected from CP induced apoptosis (E). * indicates p<.05.CC BY · PubMed Central
Figure 3 Midlife humanin treatment improves metabolic health in mice. Twice weekly treatment with HNG in midlife improves weight (A) without changing food intake (B). There were also improvements in body composition with a decreased values in visceral fat (C), an increase in lean body mass (D), and no change in subcutaneous fat (E). Although there was no significant difference in lifespan with this low of a dose of humanin (F), there was a significant decrease in circulating IGF-I (G) and a trend (p<.1) for leptin (H). *indicates p<.05 +indicates p<.10.
Figure 3 Midlife humanin treatment improves metabolic health in mice. Twice weekly treatment with HNG in midlife improves weight (A) without changing food intake (B). There were also improvements in body composition with a decreased values in visceral fat (C), an increase in lean body mass (D), and no change in subcutaneous fat (E). Although there was no significant difference in lifespan with this low of a dose of humanin (F), there was a significant decrease in circulating IGF-I (G) and a trend (p<.1) for leptin (H). *indicates p<.05 +indicates p<.10.CC BY · PubMed Central
Figure 4 Humanin levels are related to human mitochondrial health. Low mtDNA copy number is associated with lower levels of humanin (A). Increased mtDNA mutation or absence of mtDNA (rho0 cells) is associated with decreased levels of humanin (B). Humanin levels are also decreased in the CSF of Alzheimer’s diseases patients (n=4) compared to control (n=3) (C) *indicates p<.05.
Figure 4 Humanin levels are related to human mitochondrial health. Low mtDNA copy number is associated with lower levels of humanin (A). Increased mtDNA mutation or absence of mtDNA (rho0 cells) is associated with decreased levels of humanin (B). Humanin levels are also decreased in the CSF of Alzheimer’s diseases patients (n=4) compared to control (n=3) (C) *indicates p<.05.CC BY · PubMed Central
Figure 5 Humanin levels are correlated with longevity. HN levels decline with age in monkeys between 19 and 25 years of age but not between 25 and 35 years of age (n=40, 25, and 21 for 19, 25, and 35 years of age respectively) (A). In two rodents, the short-lived mouse (n=29) has a decline in humanin levels over the first 16 months of life, while the long-lived naked mole rat (NMR) (n=10) maintains levels over 2 decades (B). Humanin levels in offspring of centenarians (n=18), who have a higher chance of becoming centenarians themselves, are significantly higher than age-matched control levels (n=19)(C). * indicates p<.05, columns with different numbers are significantly different from each other.
Figure 5 Humanin levels are correlated with longevity. HN levels decline with age in monkeys between 19 and 25 years of age but not between 25 and 35 years of age (n=40, 25, and 21 for 19, 25, and 35 years of age respectively) (A). In two rodents, the short-lived mouse (n=29) has a decline in humanin levels over the first 16 months of life, while the long-lived naked mole rat (NMR) (n=10) maintains levels over 2 decades (B). Humanin levels in offspring of centenarians (n=18), who have a higher chance of becoming centenarians themselves, are significantly higher than age-matched control levels (n=19)(C). * indicates p<.05, columns with different numbers are significantly different from each other.CC BY · PubMed Central

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Metadata

Authors
Yen, K., Mehta, H. H., Kim, S.-J., Lue, Y., Hoang, J., Guerrero, N., Port, J., Bi, Q., Navarrete, G., Brandhorst, S., Lewis, K. N., Wan, J., Swerdloff, R., Mattison, J. A., Buffenstein, R., Breton, C. V., Wang, C., Longo, V., Atzmon, G., Wallace, D., Barzilai, N., & Cohen, P.
Affiliations
  • Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA
  • Department of Medicine, The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA
  • Department of Physiology, The Barshop Institute, University of Texas Health at San Antonio, TX 78229, USA
  • Translational Gerontology Branch, National Institute on Aging, Dickerson, MD 20892, USA
  • Department of Preventive Medicine, Keck School of Medicine, USC, Los Angeles, CA 90089, USA
  • Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA
  • Center for Mitochondrial and Epigenomic Medicine, Children’s Hospital of Philadelphia, Department of Pediatrics, Division of Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Venue
Aging
Publisher
Impact Journals, LLC
Published
2020-06-23
Volume
12
Issue
12
Pages
11185-11199
ISSN
1945-4589
DOI
10.18632/aging.103534
PMC
PMC7343442
Cited by
106
References
6
Language
en

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CoChat. (2026). Citation check: The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan. https://app.cochat.ai/papers/10.18632/aging.103534
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Yen, K., Mehta, H. H., Kim, S.-J., Lue, Y., Hoang, J., Guerrero, N., Port, J., Bi, Q., Navarrete, G., Brandhorst, S., Lewis, K. N., Wan, J., Swerdloff, R., Mattison, J. A., Buffenstein, R., Breton, C. V., Wang, C., Longo, V., Atzmon, G., . . . Cohen, P. (2020). The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan. Aging. https://doi.org/10.18632/aging.103534