bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2024–06–02
five papers selected by
Ayesh Seneviratne, Western University
  1. Novel somatic mutations in blood driving age-related clonal hematopoiesis.
  2. CHIPing away at proteomics to find correlations with myeloid neoplasms.
  3. Reducing seizures with senolytic drugs.
  4. Unlocking longevity with GLP-1: A key to turn back the clock?
  5. Senolytic Therapy Enabled by Senescent Cell-Sensitive Biomimetic Melanin Nano-senolytics.
  1. Nat Genet. 2024 May 28.
    Novel somatic mutations in blood driving age-related clonal hematopoiesis.
      
    DOI:  https://doi.org/10.1038/s41588-024-01756-0
  2. Clin Cancer Res. 2024 May 31.
    CHIPing away at proteomics to find correlations with myeloid neoplasms.
    Avni M Bhalgat, Justin Taylor.
      Plasma proteomic profiling to identify associations with myeloid neoplasm (MN) risk, highlights the potential of integrating protein and genetic biomarkers for detection individuals at high-risk of developing MN. These proteins also offer valuable insights into biological pathways and inflammatory mechanisms involved in the progression of clonal hematopoiesis (CH) to MN.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-24-0827
  3. Nat Rev Drug Discov. 2024 May 31.
    Reducing seizures with senolytic drugs.
    Sarah Crunkhorn.
      
    DOI:  https://doi.org/10.1038/d41573-024-00092-6
  4. Maturitas. 2024 May 21. pii: S0378-5122(24)00123-3. [Epub ahead of print]186 108028
    Unlocking longevity with GLP-1: A key to turn back the clock?
    Vivek P Chavda, Pankti C Balar, Dixa A Vaghela, Payal Dodiya.
      Traditionally known for managing blood sugar, GLP-1, a gut hormone, is emerging as a potential key to both lengthening lifespan and combating age-related ailments. While widely recognized for its role in blood sugar control, GLP-1 is increasingly recognized for its diverse effects on various biological pathways beyond glucose metabolism. Research across organisms and humans suggests that activating GLP-1 receptors significantly impacts cellular processes linked to aging. Its ability to boost mitochondrial function, enhance cellular stress resistance, and quell inflammation hints at its wider influence on aging mechanisms. This intricate interplay between GLP-1 and longevity appears to act through multiple pathways. One key effect is its ability to modulate insulin sensitivity, potentially curbing age-related metabolic issues like type 2 diabetes. Its neuroprotective properties also make it a promising candidate for addressing age-related cognitive decline and neurodegenerative diseases. Furthermore, preclinical studies using GLP-1 analogs or agonists have shown promising results in extending lifespan and improving healthspan in various model organisms. These findings provide a compelling rationale for exploring GLP-1-based interventions in humans to extend healthy aging. However, despite the exciting therapeutic prospects of GLP-1 in promoting longevity, challenges remain. Determining optimal dosages, establishing long-term safety profiles, and investigating potential adverse effects require comprehensive clinical investigations before we can confidently translate these findings to humans. This article emphasises the wide applicability of GLP-1.
    Keywords:  Age-related diseases; Bone health; Cancer; Cardiovascular health; Cellular senescence; Cognitive function; Frailty; GLP-1; Glucagon-like peptide-1; Healthy aging; Incretin hormones; Insulin sensitivity; Longevity; Metabolic health; Mitochondrial dysfunction; Neuroprotective effects; Sarcopenia
    DOI:  https://doi.org/10.1016/j.maturitas.2024.108028
  5. Adv Healthc Mater. 2024 May 26. e2401085
    Senolytic Therapy Enabled by Senescent Cell-Sensitive Biomimetic Melanin Nano-senolytics.
    Hairui Zhang, Xiaoling Xu, Xin Shou, Wucan Liao, Chengkang Jin, Changjiang Chen, Chen Zhang, Wenhua Gao, Junfeng Zhang, Weihong Ge, Liyun Shi.
      Cellular senescence is a significant risk factor for aging and age-related diseases (ARD). The canonical senolytics Dasatinib and Quercetin (DQ) have shown promise in clearing senescent cells (SnCs); however, the lack of selectivity poses a challenge in achieving optimal outcomes. Despite the recent occurrence of the nanomaterial-based approaches targeting SnCs, limited therapeutic effects and potential toxicity still remain a major concern. Herein, we developed a "double locks-like" nanoplatform that integrated Galactan coating and mesoporous polydopamine to encase the senolytic drug DQ. By this way, DQ was only released in SnCs that were featured with higher levels of β-galactosidase (β-gal) and low PH. Additionally, the nanoparticles were equipped with 2,2,6,6-Tetramethylpiperidine-1-oxyl (Tempo) to gain enhanced photothermal converting potential. Consequently, the synthesized nanosenolytics demonstrated remarkable specificity and efficacy in eradicating SnCs, and accordingly reversed pulmonary fibrosis in mice without affecting normal tissues. Upon exposure of near-infrared (NIR) light, the nanoparticles demonstrated to efficiently remove senescent tumor cells inducted by chemotherapy, thereby hindering the outgrowth and metastasis or breast cancer. Collectively, the present study develops an "On/Off" switchable nanoplatform in response to SnCs, and produces a more safe, efficient and feasible way to delay aging or alleviate age-associated diseases. This article is protected by copyright. All rights reserved.
    Keywords:  Dasatinib and Quercetin; Pulmonary fibrosis; Targeting senescent cells; breast cancer; β‐galactosidase; “On/Off” switchable nanoplatform
    DOI:  https://doi.org/10.1002/adhm.202401085
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