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. 2020 Jul 13;22(3):2155–2162. doi: 10.3892/mmr.2020.11339

Table I.

Evidence of the possible genes or biomarkers in patients with POP, compared with normal dermal fibroblast.

Types of aging Evidence in vitro culture Evidence ex vivo from patients with POP Evidence in vivo from the dermal fibroblasts in the elderly
Genome instability
  HOXA11, HOXA13, ESR1 and ESR2 Y (49) Y (62) ND
  γH2AX foci Y (50) Y (17) Y (16)
  Mutant NER Y (59) ND ND
  Replicative activity Y (60) ND ND
  Telomere shortening Y (61,62) Y (63) ND
  Telomere damage Y (50) ND Y (16)
Mitochondrial dysfunction
  mtDNA mutations Y (64,65) ND ND
  Altered fusion ND Y (67) ND
  Increasing mitogenesis Y (69,70) ND
Cell senescence
  p16INK4A Y (71) ND Y (66,67)
  p21 Y (72,73) Y (78) ND
  p53 ND Y (78) ND
  SASP Y (74) Y (74) ND
  SAHF Y (75,76) ND Y (68)
  γH2AX foci Y (50) ND Y (16)
Imbalanced proteostasis
  Chaperon dysfunction ND Y (78) ND
  Proteasome activity Y (42,77) ND ND
  Decreased autophagy ND ND ND
  Increased MMP secretion Y (43) Y (39) Y (39)
Stem cell exhaustion
  Regeneration potential ND ND ND

HOXA11, homeobox A11; HOXA13, homeobox A13; Y, evidence confirmed; ND, no data; ESR1, estrogen receptor 1; ESR2, estrogen receptor 2; γH2AX, H2AX histone protein phosphorylated at the serine-139 position; NER, nucleotide excision repair; SASP, senescence-associated secretory phenotype; SAHF, senescence-associated heterochromatin aggregation; MMP, matrix metalloprotein; mtDNA, mitochondrial DNA.