ReviewFrontiers in endocrinology2022
Cellular Senescence in Diabetes Mellitus: Distinct Senotherapeutic Strategies for Adipose Tissue and Pancreatic β Cells.
Review in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 112 citations in OpenAlex.
- Effect of henagliflozin on aging biomarkers in patients with type 2 diabetes: A multicenter, randomized, double-blind, placebo-controlled study.Cell reports. Medicine · 2025Trial
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- CBX4 stabilizes NEUROD1 through SUMO-ubiquitin crosstalk to delay β-cell senescence.Nature communications · 2026Article
- β-cell FMO3-produced TMAO prevents NF-κB-mediated senescence and inflammation in ageing and diabetic conditions.Nature communications · 2026Article
- SenSet defines cell-type specific senescence signatures in the aged human lung.The EMBO journal · 2026Article
- Identification and validation of lactylation-related diagnostic biomarkers for type 2 diabetes by WGCNA.Journal of clinical biochemistry and nutrition · 2026Article
- Exploring the Senotherapeutic Potential of Polyphenols in Aging and Disease: A Literature Review.International journal of molecular sciences · 2026Review
- Influencing factors and predictive model construction of perioperative blood glucose fluctuations in patients with coronary heart disease complicated with type 2 diabetes mellitus undergoing percutaneous coronary intervention.BMC endocrine disorders · 2026Article
- Type 2 Diabetes Mellitus as a Multisystem Disease: From Insulin Resistance to Organ Crosstalk-A Narrative Review.Biomedicines · 2026Review
- Review
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
- Cavin gene family and caveolae-related disorders: pathogenetic roles and possible mechanisms.Cell communication and signaling : CCS · 2026Review
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Cellular senescence and metabolic aging in type 2 diabetes: mechanistic insights and translational implications.Frontiers in endocrinology · 2026Review
- Chronic inflammation as a driving factor for sarcopenia: an update on pathophysiology and future therapeutic targets.Frontiers in pharmacology · 2026Review
- Effects of Chlorogenic Acid on Cellular Senescence in an In Vitro Model of 3T3-L1 Murine Adipocytes.Molecules (Basel, Switzerland) · 2026Article
- Metformin Mitigates Diabetes-Driven Renal Senescence via Immunomodulation and the FABP4/FOXO1 Axis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cellular senescence and polycystic ovary syndrome: mechanisms and therapeutic strategies from a new perspective.Annals of medicine · 2025Review
- Unleashing endogenous regeneration by senolytics.Journal of translational medicine · 2025Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased insulin resistance and impaired insulin secretion are significant characteristics manifested by patients with type 2 diabetes mellitus (T2DM). The degree and extent of these two features in T2DM vary among races and individuals. Insulin resistance is accelerated by obesity and is accompanied by accumulation of dysfunctional adipose tissues. In addition, dysfunction of pancreatic β-cells impairs insulin secretion. T2DM is significantly affected by aging, as the β-cell mass diminishes with age. Moreover, both obesity and hyperglycemia-related metabolic changes in developing diabetes are associated with accumulation of senescent cells in multiple organs, that is, organismal aging. Cellular senescence is defined as a state of irreversible cell cycle arrest with concomitant functional decline. It is caused by telomere shortening or senescence-inducing stress. Senescent cells secrete proinflammatory cytokines and chemokines, which is designated as the senescence-associated secretory phenotype (SASP), and this has a negative impact on adipose tissues and pancreatic β-cells. Recent advances in aging research have suggested that senolysis, the removal of senescent cells, can be a promising therapeutic approach to prevent or improve aging-related diseases, including diabetes. The attenuation of a SASP may be beneficial, although the pathophysiological involvement of cellular senescence in diabetes is not fully understood. In the clinical application of senotherapy, tissue-context-dependent senescent cells are increasingly being recognized as an issue to be solved. Recent studies have observed highly heterogenic and complex senescent cell populations that serve distinct roles among tissues, various stages of disease, and different ages. For example, in high-fat-diet induced diabetes with obesity, mouse adipose tissues display accumulation of
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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.