ArticleThe Journal of biological chemistry2015
Inflammation and pyroptosis mediate muscle expansion in an interleukin-1β (IL-1β)-dependent manner.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Exploring the association between weight-adjusted-waist index and overactive bladder: A population-based study.Medicine · 2026Article
- GLI1 Promotes Hypoxia Induced Pyroptosis of PASMCs and Aggravates Pulmonary Arterial Hypertension in Rats by Upregulating HDAC1 Expression.Cardiovascular toxicology · 2026Article
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Pulmonary artery smooth muscle cell pyroptosis promotes the proliferation of PASMCs by paracrine IL‑1β and IL‑18 in monocrotaline‑induced pulmonary arterial hypertensive rats.Experimental and therapeutic medicine · 2024Article
- Integrated insulin-iron nanoparticles: a multi-modal approach for receptor-specific bioimaging, reactive oxygen species scavenging, and wound healing.Discover nano · 2024Article
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- Why Are Some People with Lower Urinary Tract Symptoms (LUTS) Depressed? New Evidence That Peripheral Inflammation in the Bladder Causes Central Inflammation and Mood Disorders.International journal of molecular sciences · 2023Review
- Ghost messages: cell death signals spread.Cell communication and signaling : CCS · 2023Review
- Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity.American journal of physiology. Renal physiology · 2022Article
- Spotlight on pyroptosis: role in pathogenesis and therapeutic potential of ocular diseases.Journal of neuroinflammation · 2022Review
- Diabetic bladder dysfunction progresses from an overactive to an underactive phenotype in a type-1 diabetic mouse model (Akita female mouse) and is dependent on NLRP3.Life sciences · 2022Article
- microRNA-126 inhibits vascular cell adhesion molecule-1 and interleukin-1beta in human dental pulp cells.Journal of clinical laboratory analysis · 2022Article
- Inflammation triggered by the NLRP3 inflammasome is a critical driver of diabetic bladder dysfunction.Frontiers in physiology · 2022Review
- Stem Cell-Derived Exosomes Ameliorate Doxorubicin-Induced Muscle Toxicity through Counteracting Pyroptosis.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Zingerone [4-(3-Methoxy-4-hydroxyphenyl)-butan-2] Attenuates Lipopolysaccharide-Induced Inflammation and Protects Rats from Sepsis Associated Multi Organ Damage.Molecules (Basel, Switzerland) · 2020Article
- Identification of NLRP3 Inflammation-Related Gene Promoter Hypomethylation in Diabetic Retinopathy.Investigative ophthalmology & visual science · 2020Article
- Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- P38 MAPK signaling pathway mediates COM crystal-induced crystal adhesion change in rat renal tubular epithelial cells.Urolithiasis · 2020Article
- Periodontal inflammation recruits distant metastatic breast cancer cells by increasing myeloid-derived suppressor cells.Oncogene · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Muscle inflammation is often associated with its expansion. Bladder smooth muscle inflammation-induced cell death is accompanied by hyperplasia and hypertrophy as the primary cause for poor bladder function. In mice, DNA damage initiated by chemotherapeutic drug cyclophosphamide activated caspase 1 through the formation of the NLRP3 complex resulting in detrusor hyperplasia. A cyclophosphamide metabolite, acrolein, caused global DNA methylation and accumulation of DNA damage in a mouse model of bladder inflammation and in cultured bladder muscle cells. In correlation, global DNA methylation and NLRP3 expression was up-regulated in human chronic bladder inflammatory tissues. The epigenetic silencing of DNA damage repair gene, Ogg1, could be reversed by the use of demethylating agents. In mice, demethylating agents reversed cyclophosphamide-induced bladder inflammation and detrusor expansion. The transgenic knock-out of Ogg1 in as few as 10% of the detrusor cells tripled the proliferation of the remaining wild type counterparts in an in vitro co-culture titration experiment. Antagonizing IL-1β with Anakinra, a rheumatoid arthritis therapeutic, prevented detrusor proliferation in conditioned media experiments as well as in a mouse model of bladder inflammation. Radiation treatment validated the role of DNA damage in the NLRP3-associated caspase 1-mediated IL-1β secretory phenotype. A protein array analysis identified IGF1 to be downstream of IL-1β signaling. IL-1β-induced detrusor proliferation and hypertrophy could be reversed with the use of Anakinra as well as an IGF1 neutralizing antibody. IL-1β antagonists in current clinical practice can exploit the revealed mechanism for DNA damage-mediated muscular expansion.
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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.