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529 results on '"Wondisford, Fredric"'

35. Single-cell profiling of brain pericyte heterogeneity following ischemic stroke unveils distinct pericyte subtype-targeted neural reprogramming potential and its underlying mechanisms.

Author

Loan, Allison, Awaja, Nidaa, Lui, Margarita, Syal, Charvi, Sun, Yiren, Sarma, Sailendra N., Chona, Ragav, Johnston, William B., Cordova, Alex, Saraf, Devansh, Nakhlé, Anabella, O'Connor, Kaela, Thomas, Jacob, Leung, Joseph, Seegobin, Matthew, Ling He, Wondisford, Fredric E., Picketts, David J., Tsai, Eve C., and Hing Man Chan

Published
2024
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39. Targeting hepatic kisspeptin receptor ameliorates nonalcoholic fatty liver disease in a mouse model

Author

Guzman, Stephania, Dragan, Magdalena, Kwon, Hyokjoon, Oliveira, Vanessa de, Rao, Shivani, Bhatt, Vrushank, Kalemba, Katarzyna M., Shah, Ankit, Rustgi, Vinod K., Wang, He, Bech, Paul R., Abbara, Ali, Izzi-Engbeaya, Chioma, Manousou, Pinelopi, Guo, Jessie Y., Guo, Grace L., Radovick, Sally, Dhillo, Waljit S., Wondisford, Fredric E., Babwah, Andy V., and Bhattacharya, Moshmi

Subjects
Fatty liver -- Models -- Care and treatment, Cellular signal transduction -- Research, Neuropeptides -- Health aspects, Cell receptors -- Health aspects, Molecular targeted therapy -- Research, Health care industry
Abstract

Nonalcoholic fatty liver disease (NAFLD), the most common liver disease, has become a silent worldwide pandemic. The incidence of NAFLD correlates with the rise in obesity, type 2 diabetes, and metabolic syndrome. A hallmark feature of NAFLD is excessive hepatic fat accumulation or steatosis, due to dysregulated hepatic fat metabolism, which can progress to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Currently, there are no approved pharmacotherapies to treat this disease. Here, we have found that activation of the kisspeptin 1 receptor (KISS1R) signaling pathway has therapeutic effects in NAFLD. Using high-fat diet-fed mice, we demonstrated that a deletion of hepatic Kiss1r exacerbated hepatic steatosis. In contrast, enhanced stimulation of KISS1R protected against steatosis in wild-type C57BL/6J mice and decreased fibrosis using a diet-induced mouse model of NASH. Mechanistically, we found that hepatic KISS1R signaling activates the master energy regulator, AMPK, to thereby decrease lipogenesis and progression to NASH. In patients with NAFLD and in high-fat diet-fed mice, hepatic KISS1/KISS1R expression and plasma kisspeptin levels were elevated, suggesting a compensatory mechanism to reduce triglyceride synthesis. These findings establish KISS1R as a therapeutic target to treat NASH., Introduction The liver is the principal organ involved in lipid metabolism. Dyslipidemia leads to metabolic disorders such as nonalcoholic fatty liver disease (NAFLD), which has become an increasing global public [...]

Published
2022
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