Evidence map›Paper›PMID 26948035›Full record

ReviewThe Canadian journal of cardiology2016

Sirtuins, Cell Senescence, and Vascular Aging.

Yujiro Kida, Michael S Goligorsky

Open access · greenAbstract readReview
In one paragraph

Review in The Canadian journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 254 citations in OpenAlex.

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97 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Yujiro KidaDepartments of Medicine, Pharmacology, and Physiology, Renal Research Institute, New York Medical College, Valhalla, New York, USA. Electronic address: yujiro_kida@nymc.edu.
Michael S GoligorskyDepartments of Medicine, Pharmacology, and Physiology, Renal Research Institute, New York Medical College, Valhalla, New York, USA.
New York Medical College · USRenal Research Institute · US

Funding

RENAL ENDOTHELIAL AND SMOOTH MUSCLE CELLS INTERACTIONSR01DK045462 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI GOLIGORSKY, MICHAEL S · 1995 to 2014
$4.8M
VASCULAR PERMEABILITY IN DIABETIC NEPHROPATHYR01DK054602 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI GOLIGORSKY, MICHAEL S · 1999 to 2010
$2.5M
Endothelial dysfunction in acute renal ischemiaR01DK052783 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI GOLIGORSKY, MICHAEL S · 1997 to 2007
$2.0M
NIDDK NIH HHS R01 DK045462NIDDK NIH HHS R01 DK052783NIDDK NIH HHS R01 DK054602
6 · The paper itself

Abstract

The sirtuins (SIRTs) constitute a class of proteins with nicotinamide adenine dinucleotide-dependent deacetylase or adenosine diphosphate-ribosyltransferase activity. Seven SIRT family members have been identified in mammals, from SIRT1, the best studied for its role in vascular aging, to SIRT7. SIRT1 and SIRT2 are localized in the nucleus and cytoplasm. SIRT3, SIRT4, and SIRT5 are mitochondrial, and SIRT6 and SIRT7 are nuclear. Extensive studies have clearly revealed that SIRT proteins regulate diverse cell functions and responses to stressors. Vascular aging involves the aging process (senescence) of endothelial and vascular smooth muscle cells. Two types of cell senescence have been identified: (1) replicative senescence with telomere attrition; and (2) stress-induced premature senescence without telomere involvement. Both types of senescence induce vascular cell growth arrest and loss of vascular homeostasis, and contribute to the initiation and progression of cardiovascular diseases. Previous mechanistic studies have revealed in detail that SIRT1, SIRT3, and SIRT6 show protective functions against vascular aging, and definite vascular function of other SIRTs is under investigation. Thus, direct SIRT modulation and nicotinamide adenine dinucleotide stimulation of SIRT are promising candidates for cardiovascular disease therapy. A small number of pilot studies have been conducted to assess SIRT modulation in humans. These clinical studies have not yet provided convincing evidence that SIRT proteins alleviate morbidity and mortality in patients with cardiovascular diseases. The outcomes of multiple ongoing clinical trials are awaited to define the efficacy of SIRT modulators and SIRT activators in cardiovascular diseases, along with the potential adverse effects of chronic SIRT modulation.

Indexed as

AgingCardiovascular DiseasesCell SurvivalCellular SenescenceEndothelium, VascularHomeostasisHumansMyocytes, Smooth MuscleSirtuinsTelomereSirtuins

Identifiers

PMID26948035
PMCPMC4848124
OpenAlexW2196369193

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.