Evidence map›Paper›PMID 33805567›Full record

ReviewInternational journal of molecular sciences2021

Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.

Abhishek Chandra, Jyotika Rajawat

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 4 pooled it
17.3field-weighted citation impact, top 1% 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, 4 syntheses or guidelines pooled it, 231 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Consequences of Aging on Bone.Aging and disease · 2023
    Pooled it
  5. Trial
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
  13. A genomic structural equation modelling analysis of the shared genetic architecture of the aging spine.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
    Article
  14. Article
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article

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 2 countries.

Abhishek ChandraDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55902, USA.
Jyotika RajawatDepartment of Zoology, University of Lucknow, University Rd, Babuganj, Hasanganj, Lucknow, Uttar Pradesh 226007, India.
Mayo Clinic in Arizona · USUniversity of Lucknow · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone is a dynamic organ maintained by tightly regulated mechanisms. With old age, bone homeostasis, which is maintained by an intricate balance between bone formation and bone resorption, undergoes deregulation. Oxidative stress-induced DNA damage, cellular apoptosis, and cellular senescence are all responsible for this tissue dysfunction and the imbalance in the bone homeostasis. These cellular mechanisms have become a target for therapeutics to treat age-related osteoporosis. Genetic mouse models have shown the importance of senescent cell clearance in alleviating age-related osteoporosis. Furthermore, we and others have shown that targeting cellular senescence pharmacologically was an effective tool to alleviate age- and radiation-induced osteoporosis. Senescent cells also have an altered secretome known as the senescence associated secretory phenotype (SASP), which may have autocrine, paracrine, or endocrine function. The current review discusses the current and potential pathways which lead to a senescence profile in an aged skeleton and how bone homeostasis is affected during age-related osteoporosis. The review has also discussed existing therapeutics for the treatment of osteoporosis and rationalizes for novel therapeutic options based on cellular senescence and the SASP as an underlying pathogenesis of an aging bone.

Indexed as

AgingAnimalsBone and BonesCellular SenescenceDNA DamageEpigenesis, GeneticGenomic InstabilityHumansMitochondriaOsteoporosisParathyroid HormonePoly (ADP-Ribose) Polymerase-1TelomereParathyroid HormonePoly (ADP-Ribose) Polymerase-1agingosteoporosisradiationSASPsenescencesenotherapeutic

Identifiers

PMID33805567
PMCPMC8037620
OpenAlexW3140129245

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.