Evidence map›Paper›PMID 40715742›Full record

ReviewInflammopharmacology2025

Immunopharmacology of senescence: targeting the senescence-associated secretory phenotype (SASP)-a mechanism-based review.

Poonam Sahu, Trilochan Satapathy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Journal of pharmacopuncture · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Stem Cells in Aging and Anti-Aging.Stem cell reviews and reports · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Stem cells in organogenesis and regeneration.Stem cell research & therapy · 2026
    Review
  13. Review
  14. Review
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.

Poonam SahuColumbia Institute of Pharmacy, Vill-Tekari, Near Vidhansabha, Raipur, 493111, Chhattisgarh, India. poonamsahu152@gmail.com.ORCID http://orcid.org/0000-0003-4398-003X
Trilochan SatapathyColumbia Institute of Pharmacy, Vill-Tekari, Near Vidhansabha, Raipur, 493111, Chhattisgarh, India.ORCID http://orcid.org/0000-0001-6871-1288

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a natural process, where cells permanently stop dividing in response to stress, helping prevent cancer and assist in tissue repair. However, these senescent cells release a variety of inflammatory factors, known as the senescence-associated secretory phenotype (SASP), which, when persistent, can cause chronic inflammation, disrupt the immune system, and contribute to aging and related diseases. How the immune system interacts with these cells plays a big role in whether they are cleared or cause harm, making immunopharmacology-a field that studies how drugs affect immune responses-an exciting way to develop new treatments. This review brings together the latest research on how the immune system engages with senescent cells, the drugs that can target SASP, and new therapies that either remove these cells or change their harmful secretions. Our goal is to provide a clear overview of these advances and challenges to guide future development of therapies aimed at improving health and treating age-related conditions by targeting the SASP.

Indexed as

AgingCellular SenescenceSenescence-Associated Secretory PhenotypeAnimalsHumansImmune SystemInflammationCellular senescenceImmunosuppressionSenolyticsSenomorphicsTissue remodeling

Identifiers

What OpenQuestion holds

Textmetadata
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.