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Artery disease and diabetic foot ulcers share gene-activity patterns

An analysis of human gene-activity datasets identified 72 genes shared by both conditions and associated with senescence, a state in which cells stop dividing.

Paper by Fuguang Zhang, Heng Wang, Yuelu Yang, 3 more authorsJianwu Chen · General Hospital of Southern Theater Command
Figure 1. Cellular senescence is a common pathological feature of diabetic foot and atherosclerosis.
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Figure 1. Cellular senescence is a common pathological feature of diabetic foot and atherosclerosis.Cellular senescence is a common pathological feature of diabetic foot and atherosclerosis.Zhang et al.
Preprint: computational study of people with atherosclerosis or diabetic foot ulcersBiomarkers

Limit: Independent tissue validation included only 22 patients with foot ulcers

Edited by Boris Djordjevic · AgingResearch.News

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Researchers analyzed human gene-activity datasets for atherosclerosis, the buildup of plaque in arteries, and diabetic foot ulcers. The preprint combined observational analyses with experiments in cells grown in the lab. They compared genes whose activity differed in each disease with a list associated with senescence, a state in which cells stop dividing. Machine learning selected three genes from the 72 shared candidates.

In an independent group of 22 patients, tissue from 11 people with diabetic foot ulcers showed more senescent cells and altered activity of the selected genes compared with tissue from 11 people with non-diabetic foot ulcers. In separate experiments in fibroblasts—connective-tissue cells grown in the lab—metformin reduced senescence induced by hydrogen peroxide or high glucose and fat levels. It also partly reversed activity changes in the three selected genes.

Why it matters

The authors identify the senescence-related genes as potential diagnostic and therapeutic targets for these vascular complications of diabetes.

Caveats

The observational findings do not show that the shared gene pattern causes either disease. The preprint has not been peer-reviewed, and the metformin findings came from cells grown in the lab, not patients.

Where the evidence stands

Metformin

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

No results posted: trials that ended over a year ago with no results on ClinicalTrials.gov and no paper reporting them.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

  • 519 independent labs in 65 countries
  • 238 findings against
  • 1,476 trials, 628 with no results posted
  • Funders: National Institutes of Health and others
  • 172 of 2,406 findings with company ties
  • 195 of 1,476 trials sponsored by its developers

Cellular senescence

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

No results posted: trials that ended over a year ago with no results on ClinicalTrials.gov and no paper reporting them.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 854 independent labs in 75 countries
  • 515 findings against
  • 51 trials, 15 with no results posted
  • Funders: National Natural Science Foundation of China and others
  • 662 of 9,827 findings with company ties
  • 49 of 51 trials sponsored by developers of drugs on it

Comments

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Metformin is part of Bryan Johnson's Blueprint and David Sinclair's daily regimen in Lifespan

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