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Humanin

HN, S14G-Humanin

Quick Stats
Studies 491
Trials 100
Score 2
2021 pubmed 31 citations

Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Age Related Macular Degeneration, Role in Pathophysiology, and Possible New Therapeutic Strategies.

Bilbao-Malavé. Valentina V; González-Zamora. Jorge J; de la Puente. Miriam M; Recalde. Sergio S; Fernandez-Robredo. Patricia P; Hernandez. María M; Layana. Alfredo Garcia AG; Saenz de Viteri. Manuel M

Key Findings

  • Mitochondrial dysfunction and endoplasmic reticulum stress are key drivers of AMD pathology.
  • Humanin is listed among antioxidants that could reduce oxidative damage in the retina.
  • Current AMD treatments focus on VEGF inhibitors, but new antioxidant strategies are being explored.

Practical Outcomes

  • Humanin may be worth adding to a broader antioxidant protocol for eye health, but the evidence is still early and mostly theoretical. Biohackers should treat it as an experimental supplement, start with low doses if using a commercial source, and watch for any research updates before expecting strong benefits.

Summary

This review says that problems in mitochondria and the cell’s stress system help cause age‑related macular degeneration (AMD). It notes that several antioxidants, including the peptide humanin, might protect eye cells by easing this stress, but it doesn’t give any specific dosing or treatment plan.

Abstract

Age related macular degeneration (AMD) is the main cause of legal blindness in developed countries. It is a multifactorial disease in which a combination of genetic and environmental factors contributes to increased risk of developing this vision-incapacitating condition. Oxidative stress plays a central role in the pathophysiology of AMD and recent publications have highlighted the importance of mitochondrial dysfunction and endoplasmic reticulum stress in this disease. Although treatment with vascular endothelium growth factor inhibitors have decreased the risk of blindness in patients with the exudative form of AMD, the search for new therapeutic options continues to prevent the loss of photoreceptors and retinal pigment epithelium cells, characteristic of late stage AMD. In this review, we explain how mitochondrial dysfunction and endoplasmic reticulum stress participate in AMD pathogenesis. We also discuss a role of several antioxidants (bile acids, resveratrol, melatonin, humanin, and coenzyme Q10) in amelioration of AMD pathology.

Study Information

Provider

pubmed

Year

2021

Date

2021-07-23T00:00:00.000Z

DOI

10.3390/antiox10081170

Citations

31

References

208