Humanin G (HNG) protects age-related macular degeneration (AMD) transmitochondrial ARPE-19 cybrids from mitochondrial and cellular damage.

Nashine S, Cohen P, Chwa M, Lu S, Nesburn AB, Kuppermann BD, Kenney MC

Cell death & disease20 Jul 2017Cited by 85 (Europe PMC)

PMID28726777PMCIDPMC5550888DOI10.1038/cddis.2017.348PepBankPUB-28726777

Summary

Age-related macular degeneration (AMD) ranks third among the leading causes of visual impairment with a blindness prevalence rate of 8.7%. Despite several treatment regimens, such as anti-angiogenic drugs, laser therapy, and vitamin supplementation, being available for wet AMD, to date there are no FDA-approved therapies for dry AMD. Substantial evidence implicates mitochondrial damage and retinal pigment epithelium (RPE) cell death in the pathogenesis of AMD. However, the effects of AMD mitochondria and Humanin G (HNG), a more potent variant of the mitochondrial-derived peptide (MDP) Humanin, on retinal cell survival have not been elucidated. In this study, we characterized mitochondrial and cellular damage in transmitochondrial cybrid cell lines that contain identical nuclei but possess mitochondria from either AMD or age-matched normal (Older-normal (NL)) subjects. AMD cybrids showed (1) reduced levels of cell viability, lower mtDNA copy numbers, and downregulation of mitochondrial replication/transcription genes and antioxidant enzyme genes; and (2) elevated levels of genes related to apoptosis, autophagy and ER-stress along with increased mtDNA fragmentation and higher susceptibility to amyloid-β-induced toxicity compared to NL cybrids. In AMD cybrids, HNG protected the AMD mitochondria, reduced pro-apoptosis gene and protein levels, upregulated gp130 (a component of the HN receptor complex), and increased the protection against amyloid-β-induced damage. In summary, in cybrids, damaged AMD mitochondria mediate cell death that can be reversed by HNG treatment. Our results also provide evidence of Humanin playing a pivotal role in protecting cells with AMD mitochondria. In the future, it may be possible that AMD patient's blood samples containing damaged mitochondria may be useful as biomarkers for this condition. In conclusion, HNG may be a potential therapeutic target for treatment of dry AMD, a debilitating eye disease that currently has no available treatment. Further studies are needed to establish HNG as a viable mitochondria-targeting therapy for dry AMD.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Mechanism
In ARPE-19 cybrids with AMD mitochondria, HNG protected the AMD mitochondria.
In plain wordsIn lab-grown eye cells carrying AMD mitochondria, HNG protected the mitochondria.
Peptide
Humanin
Outcome
Direction not reportedProtection of AMD mitochondria
Study
humann: not reported in source
ARPE-19 transmitochondrial cybrids with AMD mitochondria
Outcome group
Mitochondrial function · Eye
Studied dose
Dose not stated
Source sentences
Summary
In AMD cybrids, HNG protected the AMD mitochondria, reduced pro-apoptosis gene and protein levels, upregulated gp130 (a component of the HN receptor complex), and increased the protection against amyloid-β-induced damage.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we characterized mitochondrial and cellular damage in transmitochondrial cybrid cell lines that contain identical nuclei but possess mitochondria from either AMD or age-matched normal (Older-normal (NL)) subjects.
Show in the study text Report a problemFND-2872677701
02LabIn vitro (cells)Mechanism
In ARPE-19 cybrids with AMD mitochondria, HNG reduced pro-apoptosis gene and protein levels.
In plain wordsIn lab-grown eye cells carrying AMD mitochondria, HNG lowered gene and protein levels linked to cell death.
Peptide
Humanin
Outcome
DecreasePro-apoptosis gene and protein levels
Study
humann: not reported in source
ARPE-19 transmitochondrial cybrids with AMD mitochondria
Outcome group
Neuroprotection · Eye
Studied dose
Dose not stated
Source sentences
Summary
In AMD cybrids, HNG protected the AMD mitochondria, reduced pro-apoptosis gene and protein levels, upregulated gp130 (a component of the HN receptor complex), and increased the protection against amyloid-β-induced damage.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we characterized mitochondrial and cellular damage in transmitochondrial cybrid cell lines that contain identical nuclei but possess mitochondria from either AMD or age-matched normal (Older-normal (NL)) subjects.
Show in the study text Report a problemFND-2872677702
03LabIn vitro (cells)Mechanism
In ARPE-19 cybrids with AMD mitochondria, HNG upregulated gp130, a component of the humanin receptor complex.
In plain wordsIn lab-grown eye cells carrying AMD mitochondria, HNG raised gp130, a part of the humanin receptor.
Peptide
Humanin
Outcome
Increasegp130 expression
Study
humann: not reported in source
ARPE-19 transmitochondrial cybrids with AMD mitochondria
Outcome group
Receptor activity and mechanism · Eye
Studied dose
Dose not stated
Source sentences
Summary
In AMD cybrids, HNG protected the AMD mitochondria, reduced pro-apoptosis gene and protein levels, upregulated gp130 (a component of the HN receptor complex), and increased the protection against amyloid-β-induced damage.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we characterized mitochondrial and cellular damage in transmitochondrial cybrid cell lines that contain identical nuclei but possess mitochondria from either AMD or age-matched normal (Older-normal (NL)) subjects.
Show in the study text Report a problemFND-2872677703
04LabIn vitro (cells)Efficacy outcome
In ARPE-19 cybrids with AMD mitochondria, HNG increased the protection against amyloid-β-induced damage.
In plain wordsIn lab-grown eye cells carrying AMD mitochondria, HNG increased protection against amyloid-β damage.
Peptide
Humanin
Outcome
IncreaseProtection against amyloid-β-induced damage
Study
humann: not reported in source
ARPE-19 transmitochondrial cybrids with AMD mitochondria
Outcome group
Neuroprotection · Eye
Studied dose
Dose not stated
Source sentences
Summary
In AMD cybrids, HNG protected the AMD mitochondria, reduced pro-apoptosis gene and protein levels, upregulated gp130 (a component of the HN receptor complex), and increased the protection against amyloid-β-induced damage.
1 context sentence(design, population, supporting numbers)
Summary · context
In this study, we characterized mitochondrial and cellular damage in transmitochondrial cybrid cell lines that contain identical nuclei but possess mitochondria from either AMD or age-matched normal (Older-normal (NL)) subjects.
Show in the study text Report a problemFND-2872677704

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Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

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