Eliaz Therapeutics articles
Annotations
- Kidney toxicity is a significant side-effect withGal-3 plays an essential role in kidney fibrosis and renal failure, and it is one of the critical factors for renal injury
- Inhibition of Gal-3, mediated by MCP, antagonized the pro-apoptotic (cell death) effects.
- MCP- treated mice demonstrated increased renal function and reduced renal fibrosis after cisplatin- induced MCP-treated mice showed decreased renal fibrosis and apop
Hong Yan L;Shen Yang;Jing Chun Li;Jian Xun Feng;Hong Yan L;Shen Yang;Jing Chun Li;Jian Xun Feng
Purpose: We evaluated Galectin-3 (Gal-3) as a potential early biomarker of acute kidney disease (AKI), and the effect of Gal-3 inhibition by modified citrus pectin (P-MCP) on renal ischemia/reperfusion (I/R) induced AKI.
Methods: Among fifty-two post-cardiac surgery patients, serum and urine Gal-3 levels were examined on intensive care unit (ICU) admission. In a rat renal I/R injury model, Gal-3 levels, renal
Haibing Sun;Jinyu Peng;Shuhan Cai;Qi Nie;Tianlong Li;John A. Kellum;Isaac Eliaz;Zhiyong Peng
Abstract
The invention is directed to the removal of serum gal-3 from circulation by plasmapheresis using gal-3 binding agents in either a fixed bed, or in a form easily removed, such as by being complexed with magnetic particles. This method, on its own, brings a sharp reduction and relief from the inflammation and fibroses that can be induced by circulating gal-3. The process may be combined with the administration of gal-
Background: Galectin-3 (Gal-3) is a pleiotropic glycan-binding protein shown to be involved in sepsis and acute kidney injury (AKI). However, its role has never been elucidated in sepsis-associated AKI (S-AKI). We aimed to explore Gal-3`s role and its potential utility as a therapeutic target in S-AKI.
Methods: In 57 patients admitted to the intensive care unit (ICU) with sepsis, serum Gal-3 was examined as
Haibing Sun;Huiping Jiang;Amity Eliaz;John A. Kellum;Zhiyong Peng;Isaac Eliaz
Annotations
- Acute kidney injury (AKI) is recognized as a potential risk factor for future cardiovascular events, especially heart failure.
- Up to 60% of patients with severe AKI who are admitted to an intensive care unit (ICU) die; the long-term risk of death associated with AKI is also increased.
- Preclinical models and biomarkers have identified several likely pathways, apparently involving mitochondrial injury, inflammation, cellular
Matthieu Legrand;Patrick Rossignol