Bibliografie tematiche / Alarmin HMGB1

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Letteratura scientifica selezionata sul tema "Alarmin HMGB1"

Autore: Grafiati
Pubblicato: 21 dicembre 2024

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Articoli di riviste sul tema "Alarmin HMGB1"

1

Bidwell, Joseph P., Jieping Yang, and Alexander G. Robling. "Is HMGB1 an osteocyte alarmin?" Journal of Cellular Biochemistry 103, no. 6 (2008): 1671–80. http://dx.doi.org/10.1002/jcb.21572.

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2

Palumbo, Antonino, Fabiola Atzeni, Giuseppe Murdaca, and Sebastiano Gangemi. "The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33." International Journal of Molecular Sciences 24, no. 15 (2023): 12143. http://dx.doi.org/10.3390/ijms241512143.

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Abstract (sommario):
Osteoarthritis (OA) is a multifactorial disease in which genetics, aging, obesity, and trauma are well-known risk factors. It is the most prevalent joint disease and the largest disability problem worldwide. Recent findings have described the role of damage-associated molecular patterns (DAMPs) in the course of the disease. In particular, alarmins such as HMGB1, IL-33, and S100B, appear implicated in enhancing articular inflammation and favouring a catabolic switch in OA chondrocytes. The aims of this review are to clarify the molecular signalling of these three molecules in OA pathogenesis, t
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3

Casciaro, Marco, Eleonora Di Salvo, and Sebastiano Gangemi. "HMGB-1 in Psoriasis." Biomolecules 12, no. 1 (2021): 60. http://dx.doi.org/10.3390/biom12010060.

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Abstract (sommario):
Psoriasis is a multifactorial pathology linked to systemic inflammation. Enhanced keratinocytes proliferation and a minor maturation state of the cells are typical features. Perivascular T cells, dendritic cells, macrophages, and neutrophilic granulocytes are part of the scenario completed by apoptosis dysregulation. Several proinflammatory mediators, alarmins and growth factors are increased too, both in the skin and the patients’ blood. HMGB1 is important as an alarmin in several inflammatory conditions. Released after cellular damage, HMGB1 acts as a danger signal. Several studies have cons
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Jiang, Lili, Yijia Shao, Yao Tian, Changsheng Ouyang, and Xiaohua Wang. "Nuclear Alarmin Cytokines in Inflammation." Journal of Immunology Research 2020 (December 4, 2020): 1–8. http://dx.doi.org/10.1155/2020/7206451.

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Abstract (sommario):
Pathogen-associated molecular patterns (PAMPs) are some nonspecific and highly conserved molecular structures of exogenous specific microbial pathogens, whose products can be recognized by pattern recognition receptor (PRR) on innate immune cells and induce an inflammatory response. Under physiological stress, activated or damaged cells might release some endogenous proteins that can also bind to PRR and cause a harmful aseptic inflammatory response. These endogenous proteins were named damage-associated molecular patterns (DAMPs) or alarmins. Indeed, alarmins can also play a beneficial role i
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Davalos, Albert R., Misako Kawahara, Gautam K. Malhotra, et al. "p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes." Journal of Cell Biology 201, no. 4 (2013): 613–29. http://dx.doi.org/10.1083/jcb.201206006.

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Abstract (sommario):
Cellular senescence irreversibly arrests proliferation in response to potentially oncogenic stress. Senescent cells also secrete inflammatory cytokines such as IL-6, which promote age-associated inflammation and pathology. HMGB1 (high mobility group box 1) modulates gene expression in the nucleus, but certain immune cells secrete HMGB1 as an extracellular Alarmin to signal tissue damage. We show that nuclear HMGB1 relocalized to the extracellular milieu in senescent human and mouse cells in culture and in vivo. In contrast to cytokine secretion, HMGB1 redistribution required the p53 tumor supp
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Fonken, Laura K., Matthew G. Frank, Meagan M. Kitt, et al. "The Alarmin HMGB1 Mediates Age-Induced Neuroinflammatory Priming." Journal of Neuroscience 36, no. 30 (2016): 7946–56. http://dx.doi.org/10.1523/jneurosci.1161-16.2016.

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Galaz, Jose, Roberto Romero, Marcia Arenas-Hernandez, Bogdan Panaitescu, Robert Para, and Nardhy Gomez-Lopez. "Betamethasone as a potential treatment for preterm birth associated with sterile intra-amniotic inflammation: a murine study." Journal of Perinatal Medicine 49, no. 7 (2021): 897–906. http://dx.doi.org/10.1515/jpm-2021-0049.

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Abstract (sommario):
Abstract Objectives Preterm birth remains the leading cause of perinatal morbidity and mortality worldwide. Preterm birth is preceded by spontaneous preterm labor, which is commonly associated with sterile intra-amniotic inflammation; yet, no approved treatment exists for this clinical condition. Corticosteroids are the standard of care to improve neonatal outcomes in women at risk of preterm birth. Herein, we first validated our model of alarmin-induced preterm birth. Next, we investigated whether treatment with betamethasone could prevent preterm birth resulting from sterile intra-amniotic i
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8

Gangemi, Sebastiano, Marco Casciaro, Giovanni Trapani, et al. "Association between HMGB1 and COPD: A Systematic Review." Mediators of Inflammation 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/164913.

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Abstract (sommario):
HMGB1 is an alarmin, a protein that warns and activates inflammation. Chronic obstructive pulmonary disease (COPD) is characterised by a progressive airflow obstruction and airway inflammation. Current anti-inflammatory therapies are poorly effective in maintaining lung function and symptoms of COPD. This underlines the need for finding new molecular targets involved in disease pathogenesis in order to block pathology progression. This review aims to analyse latest advances on HMGB1 role, utilisation, and potential application in COPD. To this purpose we reviewed experimental studies that inve
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9

De Martinis, Massimo, Lia Ginaldi, Maria Maddalena Sirufo, et al. "Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review." Medicina 56, no. 3 (2020): 138. http://dx.doi.org/10.3390/medicina56030138.

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Abstract (sommario):
Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiolo
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10

WANG, ZHEN, HONG ZHOU, HUAPING ZHENG, XIU TENG, XIAOQIONG WEI, and JIONG LI. "Autophagy-based unconventional secretion of alarmin HMGB1 by keratinocytes plays a pivotal role in psoriatic skin inflammation." Journal of Immunology 202, no. 1_Supplement (2019): 59.1. http://dx.doi.org/10.4049/jimmunol.202.supp.59.1.

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Abstract (sommario):
Abstract The precise mechanism by which autophagy affects psoriasis is poorly understood. Here we show that keratinocytes (KCs) autophagy was activated in psoriatic lesions of patients and mice model, positively correlating with psoriatic severity, and could be inhibited by MAPK family (ERK, p38, JNK) inactivation, implying autophagy was associated with psoriatic inflammation. Indeed, impaired autophagy flux, caused by autophagy inhibitors or KC-specific deletion of Atg5, alleviated psoriasisform inflammation, demonstrating autophagy positively regulated psoriatic inflammation. We then found a
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Tesi sul tema "Alarmin HMGB1"

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Lorvellec, Marie. "Dialogue entre le complément C1 et l'alarmine HMGB1 dans l'inflammation." Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV033.

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Abstract (sommario):
La protéase C1s est un élément central dans l’initiation de la voie classique du système du complément. Elle était auparavant considérée comme ciblant exclusivement les protéines C2 et C4 dans cette cascade protéolytique. Des découvertes récentes ont cependant mis en lumière la présence de C1s libre constitutivement active dans certaines pathologies, suggérant un rôle plus large de cette protéase au-delà de l'activation du complément. Parmi les cibles non-canoniques identifiées de C1s figure la protéine HMGB1, initialement décrite comme une protéine nucléaire impliquéedans la condensation de l
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Sigaut, Stéphanie. "Activation microgliale : mécanismes et conséquences à long terme." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC198/document.

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Abstract (sommario):
La neuro-inflammation induite par l'inflammation systémique ou générée en réponse à une lésion cérébrale aiguë a des conséquences cliniques néfastes : elle est mise en cause dans l'aggravation des lésions cérébrales aiguës chez l'homme, aussi bien chez l'adulte que chez l'enfant. La microglie est l'effecteur cérébral principal de cette réponse inflammatoire, et peut présenter selon les situations un profil neurotoxique ou, au contraire, anti-inflammatoire et régulateur. La compréhension des mécanismes d'activation microgliale et de leurs conséquences est capitale pour une meilleure prise en ch
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Bremer, Lisa. "Hyaluronan (HA) fragments as initiators or enhancers of inflammation in arthritis." Thesis, KTH, Skolan för bioteknologi (BIO), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215225.

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Malamis, Dimitrios. "Systemic levels of inflammatory mediators in periodontitis." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1436961245.

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"Molecular Mechanisms Regulating the Activation of Eosinophils Induced by S. aureus–associated NOD2/TLR2 Ligands, Alarmin HMGB1 and Antimicrobial Peptide LL-37 in Allergic Inflammation." 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292458.

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Atti di convegni sul tema "Alarmin HMGB1"

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Fölsch, K., A. Volmari, CF Manthey, AW Lohse, S. Huber, and P. Hübener. "Intestinale Entzündung und Karzinogenese werden durch das Alarmin HMGB1 reguliert." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695395.

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Davalos, Albert R., Misako Kawahara, Gautam K. Malhotra, et al. "Abstract A3: p53-dependent release of alarmin HMGB1 is a central mediator of senescent phenotypes." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a3.

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Davalos, Albert R., Misako Kawahara, Gautam Malhotra, Christian Beausejour, Francis Rodier, and Judith Campisi. "Abstract LB-483: p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-483.

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Rozycki, Henry J., Adam Brock, Melissa Yopp, Christopher Corday, Shauna Webb-Parker, and Tsuyoshi Tanabe. "Increased CXCL2 Production From Mouse Type II Alveolar Epithelial Cells In Response To The Alarmin HMGB1." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4269.

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