ReviewOxidative medicine and cellular longevity2016
"Inflammaging" as a Druggable Target: A Senescence-Associated Secretory Phenotype-Centered View of Type 2 Diabetes.
Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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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.
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Who cites it
81 citing papers in PubMed, 124 citations in OpenAlex.
- Impact of Yoga and Meditation on Cellular Aging in Apparently Healthy Individuals: A Prospective, Open-Label Single-Arm Exploratory Study.Oxidative medicine and cellular longevity · 2017Trial
- Implantation Outcome-Specific Associations Between Stromal Senescence and the Endometrial Microbiota.Microorganisms · 2026Article
- CD8Immunity & ageing : I & A · 2026Article
- Gut Microbiota and Diabetic Complications: Potential Mechanisms, Microbial Signatures, and Clinical Implications.Microorganisms · 2026Review
- iLDA-SGCN: Identifying Associations Between Age-Related Diseases and Long Non-Coding RNAs Using Dual Graph Convolutional Networks.Aging cell · 2026Article
- The Association of Ramadan Fasting on Relative Leukocyte Telomere Length in Type 2 Diabetes Mellitus.Journal of the ASEAN Federation of Endocrine Societies · 2026Article
- Deciphering the Interlinked CXCR4-Mediated Feedback Loop Among Signaling Pathways in Diabetic Wound Healing.Current diabetes reviews · 2026Review
- Article
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Immunological biomarkers and molecular signatures in healthy aging: early dynamics of subclinical atherosclerosis in a homogeneous elderly cohort.BMC cardiovascular disorders · 2025Article
- γ-Mangostin mitigates impaired wound healing and pyroptosis in human gingival fibroblasts induced by advanced glycation end products.Journal of dental sciences · 2025Article
- Biological Age, Aging Clocks, and the Interplay with Lymphoid Neoplasms: Mechanisms and Clinical Frontiers.Lymphatics · 2025Article
- Advanced glycation end products induce inflammaging in periodontal ligament fibroblasts through RAGE/AKT/mTOR/glycolysis pathway.Acta odontologica Scandinavica · 2025Article
- Immunosenescence and the Geriatric Giants: Molecular Insights into Aging and Healthspan.Medical sciences (Basel, Switzerland) · 2025Review
- Article
- ANXA2 regulates mitochondrial function and cellular senescence of PDLCs via AKT/eNOS signaling pathway under high glucose conditions.Scientific reports · 2025Article
- Pathophysiological hallmarks in type 2 diabetes heterogeneity (review).Diabetology international · 2025Review
- Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?Antioxidants (Basel, Switzerland) · 2025Review
- Inflammatory Trajectory of Type 2 Diabetes: Novel Opportunities for Early and Late Treatment.Cells · 2024Review
- Pathology of Diabetes-Induced Immune Dysfunction.International journal of molecular sciences · 2024Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a complex phenomenon driven by a variety of molecular alterations. A relevant feature of aging is chronic low-grade inflammation, termed "inflammaging." In type 2 diabetes mellitus (T2DM), many elements of aging appear earlier or are overrepresented, including consistent inflammaging. T2DM patients have an increased death rate, associated with an incremented inflammatory score. The source of this inflammation is debated. Recently, the senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammaging in both aging and T2DM. Different pathogenic mechanisms linked to T2DM progression and complications development have been linked to senescence and SASP, that is, oxidative stress and endoplasmic reticulum (ER) stress. Here we review the latest data connecting oxidative and ER stress with the SASP in the context of aging and T2DM, with emphasis on endothelial cells (ECs) and endothelial dysfunction. Moreover, since current medical practice is insufficient to completely suppress the increased death rate of diabetic patients, we propose a SASP-centered view of T2DM as a futuristic therapeutic option, possibly opening new prospects by moving the attention from one-organ studies of diabetes complications to a wider targeting of the aging process.
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Registered trials
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.