ArticleNature communications2020
The kallikrein-kinin pathway as a mechanism for auto-control of brown adipose tissue activity.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- From endocrine to immune: therapeutic potential of brown adipose tissue in remodelling the cardiovascular immune microenvironment.Frontiers in immunology · 2026Review
- Inhibition of adipocyte lipolysis by vaspin impairs thermoregulation in vivo.Nature communications · 2025Article
- Bradykinin-bradykinin 2 receptor and oxidative stress.Annals of medicine · 2025Review
- Chaperone-mediated autophagy controls brown adipose tissue thermogenic activity.Science advances · 2025Article
- A preliminary investigation of the differences in immune responses in different strains of mice with localized allergic rhinitis tolerance models.The World Allergy Organization journal · 2025Article
- Transcriptomic signatures of cold acclimated adipocytes reveal CXCL12 as a Brown autocrine and paracrine chemokine.Molecular metabolism · 2025Article
- Unravelling the Influence of Endocrine-Disrupting Chemicals on Obesity Pathophysiology Pathways.Advances in experimental medicine and biology · 2024Review
- Reduced hepatic bradykinin degradation accounts for cold-induced BAT thermogenesis and WAT browning in male mice.Nature communications · 2023Article
- Reduced secretion of neuronal growth regulator 1 contributes to impaired adipose-neuronal crosstalk in obesity.Nature communications · 2022Article
- Article
- Identification and Validation of Novel Biomarkers and Potential Targeted Drugs in Cholangiocarcinoma: Bioinformatics, Virtual Screening, and Biological Evaluation.Journal of microbiology and biotechnology · 2022Article
- Maternal high-fat diet programs white and brown adipose tissue lipidome and transcriptome in offspring in a sex- and tissue-dependent manner in mice.International journal of obesity (2005) · 2022Article
- Bioinformatics analysis and experimental validation of differentially expressed genes in mouse articular chondrocytes treated with IL-1β using microarray data.Experimental and therapeutic medicine · 2022Article
- The evolving view of thermogenic adipocytes - ontogeny, niche and function.Nature reviews. Endocrinology · 2021Review
- A Differential Pattern of Batokine Expression in Perivascular Adipose Tissue Depots From Mice.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brown adipose tissue (BAT) is known to secrete regulatory factors in response to thermogenic stimuli. Components of the BAT secretome may exert local effects that contribute to BAT recruitment and activation. Here, we found that a thermogenic stimulus leads to enhanced secretion of kininogen (Kng) by BAT, owing to induction of kininogen 2 (Kng2) gene expression. Noradrenergic, cAMP-mediated signals induce KNG2 expression and release in brown adipocytes. Conversely, the expression of kinin receptors, that are activated by the Kng products bradykinin and [Des-Arg9]-bradykinin, are repressed by thermogenic activation of BAT in vivo and of brown adipocytes in vitro. Loss-of-function models for Kng (the circulating-Kng-deficient BN/Ka rat) and bradykinin (pharmacological inhibition of kinin receptors, kinin receptor-null mice) signaling were coincident in showing abnormal overactivation of BAT. Studies in vitro indicated that Kng and bradykinin exert repressive effects on brown adipocyte thermogenic activity by interfering the PKA/p38 MAPK pathway of control of Ucp1 gene transcription, whereas impaired kinin receptor expression enhances it. Our findings identify the kallikrein-kinin system as a relevant component of BAT thermogenic regulation that provides auto-regulatory inhibitory signaling to BAT.
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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.