Diabetes, metabolic disease, and telomere length

Cheng, Fang; Carroll, Luke; Joglekar, Mugdha V.; Januszewski, Andrzej S.; Wong, Kwun Kiu; Hardikar, Anandwardhan A.; Jenkins, Alicia J.; Ma, Rong

doi:10.1016/s2213-8587(20)30365-x

Cited by 128 publications

(96 citation statements)

References 112 publications

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“…This condition is worsened by the absence of telomerase activity which is physiologically silenced in the early post-natal stage and throughout adulthood [ 19 ]. An accelerated TL shortening is a parameter associated with an increased risk of developing cardiovascular diseases and other disorders [ 48 ]. In COVID-19, patients bearing shorter telomeres in their peripheral leukocytes have been proposed to be at risk of worse prognoses [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

Mongelli

Barbi

zamperla

et al. 2021

IJMS

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The SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokine release, and immunosuppression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called persistent post-COVID-19 syndrome (PPCS) is a common finding. In COVID-19 survivors, PPCS presents one or more symptoms: fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. In this study, a cohort of 117 COVID-19 survivors (post-COVID-19) and 144 non-infected volunteers (COVID-19-free) was analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality) compared with 3.68 ± 8.17 years for the COVID-19-free population (p < 0.0001). A significant telomere shortening parallels this finding in the post-COVID-19 cohort compared with COVID-19-free subjects (p < 0.0001). Additionally, ACE2 expression was decreased in post-COVID-19 patients, compared with the COVID-19-free population, while DPP-4 did not change. In light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID-19 condition, particularly in younger patients (< 60 years).

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Section: Discussionmentioning

confidence: 99%

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

Mongelli

Barbi

zamperla

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…This condition is worsened by the absence of telomerase activity physiologically silenced early post-natally and along adulthood (25). An accelerated TL shortening is a parameter associated with an increased risk of developing cardiovascular diseases and other disorders (51). In COVID19, patients bearing shorter telomeres in their peripheral leukocytes have been proposed to risk a worse prognosis (52).…”

Section: Discussionmentioning

confidence: 99%

Evidence for Biological Age Acceleration and Telomere Shortening in Covid19 Survivors

Mongelli

Barbi

zamperla

et al. 2021

Preprint

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Introduction & Backgroundthe SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokines release, and immunodepression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called post-COVID19 syndrome (PPCS) is a common finding. In patients who survived the SARS-CoV-2 infection, overt PPCS presents one or more symptoms such as fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. The pathophysiology of PPCS is currently poorly understood, and whether epigenetic mechanisms are involved in this process is unexplored.Methods & ResultsIn this study, a cohort of 117 COVID19 survivors (post-COVID19) and 144 non-infected volunteers (COVID19-free) were analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. Besides, telomere length (TL) and ACE2 and DPP4 receptor expression were determined. The results show a consistent biological age increase in the post-covid population (58,44 ± 14,66 ChronoAge Vs. 67,18 ± 10,86 BioAge, P<0,0001), determining a DeltaAge acceleration of 10,45 ± 7,29 years (+5.25 years above range of normality) compared to 3,68 ± 8,17 years for the COVID19-free population (P<0,0001). A significant telomere shortening parallels this finding in the post-COVID19 cohort compared to COVID19-free subjects (post-COVID19 TL: 3,03 ± 2,39 Kb vs. COVID19-free: 10,67 ± 11,69 Kb; P<0,0001). Additionally, ACE2 expression was decreased in post-COVID19 patients compare to COVID19-free, while DPP-4 did not change.ConclusionIn light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID19 condition, particularly in the younger (<60 years). Although the consequences of such modifications on the long-term clinical outcome remain unclear, they might indicate a direction to investigate the pathophysiological basis of the post-COVID19 syndrome.

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“…The elderly present shorter telomeres when compared to youths [ 7 ]. Shorter telomeres were reported to be associated with a higher risk for cardiovascular diseases and diabetes [ [8] , [9] , [10] ]. Studies also suggest that male had shorter telomere than females [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Shorter leukocyte telomere length is associated with severity of COVID-19 infection.

Santos¹,

Pimenta²,

Viana³

et al. 2021

Biochemistry and Biophysics Reports

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The infection by COVID-19 is a serious global public health problem. An efficient way to improve this disease's clinical management would be to characterize patients at higher risk of progressing to critically severe infection using prognostic biomarkers. The telomere length could be used for this purpose. Telomeres are responsible for controlling the number of maximum cell divisions. The telomere length is a biomarker of aging and several diseases. We aimed to compare leukocyte telomere length (LTL) between patients without COVID-19 and patients with different clinical severity of the infection. Were included 53 patients who underwent SARS-CoV-2 PCR divided in four groups. The first group was composed by patients with a negative diagnosis for COVID-19 (n = 12). The other three groups consisted of patients with a confirmed diagnosis of COVID-19 divided according to the severity of the disease: mild (n = 15), moderate (n = 17) and severe (n = 9). The LTL was determined by Q-PCR. The severe group had the shortest LTL, followed by the moderate group. The negative and mild groups showed no differences. There is an increase of patients with hypertension (p = 0.0099) and diabetes (p = 0.0067) in moderate and severe groups. Severe group was composed by older patients in comparison with the other three groups (p = 0.0083). Regarding sex, there was no significant difference between groups (p = 0.6279). In an ordinal regression model, only LTL and diabetes were significantly associated with disease severity. Shorter telomere length was significantly associated with the severity of COVID-19 infection, which can be useful as a biomarker or to better understand the SARS-CoV-2 pathophysiology.

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Diabetes, metabolic disease, and telomere length

Cited by 128 publications

References 112 publications

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

Evidence for Biological Age Acceleration and Telomere Shortening in Covid19 Survivors

Shorter leukocyte telomere length is associated with severity of COVID-19 infection.

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