Telomere length is maternally inherited and associated with lipid metabolism in Chinese population

Guo, Liang; Chen, Yajuan; Li, Huiqin; Yin, Fanqian; Ge, Ming-Xia; Li, Hu; Zi, Meiting; Qin, Zheng‐Hong; He, Yonghan

doi:10.18632/aging.203810

Cited by 7 publications

(5 citation statements)

References 58 publications

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“…We found that TL was shortened with age, however, TL was better maintained in females than males [149]. The study found a robust association of TL between mother and offspring, but not between father and their offspring, indicating that TL is maternally inherited [149]. Other studies have investigated the relationship between maternal TL and offspring health.…”

Section: Maternal Inheritance Of Telomere Lengthmentioning

confidence: 49%

“…Recently, we explored the associations of TL with age, gender, and clinical variables, and tested the parental effects on TL variation in 1031 Chinese individuals aged between 12 and 111 years, including 108 families with parents and their offspring. We found that TL was shortened with age, however, TL was better maintained in females than males [149]. The study found a robust association of TL between mother and offspring, but not between father and their offspring, indicating that TL is maternally inherited [149].…”

Section: Maternal Inheritance Of Telomere Lengthmentioning

confidence: 53%

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Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

Gold,

Okeke,

2023

Aging and disease

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All linear chromosomal ends have specific DNA-protein complexes called telomeres. Telomeres serve as a "molecular clock" to estimate the potential length of cell replication. Shortening of telomere length (TL) is associated with cellular senescence, aging, and various age-related diseases in humans. Here we reviewed the structure, function, and regulation of telomeres and the age-related diseases associated with telomere attrition. Among the various determinants of TL, we highlight the connection between TL and heredity to provide a new overview of genetic determinants for TL. Studies across multiple species have shown that maternal and paternal TL influence the TL of their offspring, and this may affect life span and their susceptibility to age-related diseases. Hence, we reviewed the linkage between TL and parental influences and the proposed mechanisms involved. More in-depth studies on the genetic mechanism for TL attrition are needed due to the potential application of this knowledge in human medicine to prevent premature frailty at its earliest stage, as well as promote health and longevity.

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Section: Maternal Inheritance Of Telomere Lengthmentioning

confidence: 49%

Section: Maternal Inheritance Of Telomere Lengthmentioning

confidence: 53%

Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

Gold,

Okeke,

2023

Aging and disease

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“…Our results indicate an absence of an effect of prenatal BPA exposure on liver mtDNA copy number. Telomere length shortening is another marker of aging that has been linked to oxidative stress [ 126 ], impaired lipid metabolism [ 127 ], and several diseases [ 128 ], including NAFLD [ 46 , 129 , 130 ]. Liver telomere length was not affected by prenatal BPA exposure.…”

Section: Discussionmentioning

confidence: 99%

Developmental Programming: Impact of Prenatal Exposure to Bisphenol A on Senescence and Circadian Mediators in the Liver of Sheep

Motta,

Thangaraj,

Padmanabhan

2023

Toxics

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Prenatal exposure to endocrine disruptors such as bisphenol A (BPA) plays a critical role in the developmental programming of liver dysfunction that is characteristic of nonalcoholic fatty liver disease (NAFLD). Circadian and aging processes have been implicated in the pathogenesis of NAFLD. We hypothesized that the prenatal BPA-induced fatty-liver phenotype of female sheep is associated with premature hepatic senescence and disruption in circadian clock genes. The expression of circadian rhythm and aging-associated genes, along with other markers of senescence such as telomere length, mitochondrial DNA copy number, and lipofuscin accumulation, were evaluated in the liver tissue of control and prenatal BPA groups. Prenatal BPA exposure significantly elevated the expression of aging-associated genes GLB1 and CISD2 and induced large magnitude differences in the expression of other aging genes—APOE, HGF, KLOTHO, and the clock genes PER2 and CLOCK—in the liver; the other senescence markers remained unaffected. Prenatal BPA-programmed aging-related transcriptional changes in the liver may contribute to pathological changes in liver function, elucidating the involvement of aging genes in the pathogenesis of liver steatosis.

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“…Aging and age-related diseases in humans have been linked to shortening of the telomere, a unique DNA-protein complex which covers the ends of chromosomes to avoid end fusion and maintain their stability and integrity. Interestingly, knockdown of PNPLA2 shortened the telomere length in human liver HepG2 cells, implying the association of lipid metabolism impairment with telomere shortening and aging [ 50 ] and suggesting a PEDF/PEDF-R link with preservation of telomere length and anti-aging.…”

Section: Discussionmentioning

confidence: 99%

PEDF Deletion Induces Senescence and Defects in Phagocytosis in the RPE

Rebustini

Crawford

Becerra

2022

IJMS

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The retinal pigment epithelium (RPE) expresses the Serpinf1 gene to produce pigment epithelium-derived factor (PEDF), a retinoprotective protein that is downregulated with cell senescence, aging and retinal degenerations. We determined the expression of senescence-associated genes in the RPE of 3-month-old mice that lack the Serpinf1 gene and found that Serpinf1 deletion induced H2ax for histone H2AX protein, Cdkn1a for p21 protein, and Glb1 gene for β-galactosidase. Senescence-associated β-galactosidase activity increased in the Serpinf1 null RPE when compared with wild-type RPE. We evaluated the subcellular morphology of the RPE and found that ablation of Serpinf1 increased the volume of the nuclei and the nucleoli number of RPE cells, implying chromatin reorganization. Given that the RPE phagocytic function declines with aging, we assessed the expression of the Pnpla2 gene, which is required for the degradation of photoreceptor outer segments by the RPE. We found that both the Pnpla2 gene and its protein PEDF-R declined with the Serpinf1 gene ablation. Moreover, we determined the levels of phagocytosed rhodopsin and lipids in the RPE of the Serpinf1 null mice. The RPE of the Serpinf1 null mice accumulated rhodopsin and lipids compared to littermate controls, implying an association of PEDF deficiency with RPE phagocytosis dysfunction. Our findings establish PEDF loss as a cause of senescence-like changes in the RPE, highlighting PEDF as both a retinoprotective and a regulatory protein of aging-like changes associated with defective degradation of the photoreceptor outer segment in the RPE.

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Telomere length is maternally inherited and associated with lipid metabolism in Chinese population

Cited by 7 publications

References 58 publications

Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

Developmental Programming: Impact of Prenatal Exposure to Bisphenol A on Senescence and Circadian Mediators in the Liver of Sheep

PEDF Deletion Induces Senescence and Defects in Phagocytosis in the RPE

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