Zobrazeno 1 - 10
of 94
pro vyhledávání: '"Wai W. Cheung"'
Publikováno v:
Kidney Diseases (2024)
Background: Primary hyperoxaluria (PH) is a rare autosomal recessive disorder, mainly due to the increase in endogenous oxalate production, causing a series of clinical features such as kidney stones, nephrocalcinosis, progressive impairment of renal
Externí odkaz:
https://doaj.org/article/abb67a2d9a314f63990bd7145672ab99
Autor:
Wai W. Cheung, Sheng Hao, Ronghao Zheng, Zhen Wang, Alex Gonzalez, Ping Zhou, Hal M. Hoffman, Robert H. Mak
Publikováno v:
Journal of Cachexia, Sarcopenia and Muscle, Vol 12, Iss 5, Pp 1296-1311 (2021)
Abstract Background Ctns−/− mice, a mouse model of infantile nephropathic cystinosis, exhibit hypermetabolism with adipose tissue browning and profound muscle wasting. Inflammatory cytokines such as interleukin (IL)‐1 trigger inflammatory casca
Externí odkaz:
https://doaj.org/article/65d366eed65f485ebf1f43f6c6b27094
Autor:
Wai W. Cheung, Ronghao Zheng, Sheng Hao, Zhen Wang, Alex Gonzalez, Ping Zhou, Hal M. Hoffman, Robert H. Mak
Publikováno v:
Scientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
Abstract Cytokines such as IL-6, TNF-α and IL-1β trigger inflammatory cascades which may play a role in the pathogenesis of chronic kidney disease (CKD)-associated cachexia. CKD was induced by 5/6 nephrectomy in mice. We studied energy homeostasis
Externí odkaz:
https://doaj.org/article/e4b1d33e01524a95bb59afcecfed6c92
Publikováno v:
Antioxidants, Vol 12, Iss 4, p 945 (2023)
Redox signaling alterations contribute to chronic kidney disease (CKD)-associated cachexia. This review aims to summarize studies about redox pathophysiology in CKD-associated cachexia and muscle wasting and to discuss potential therapeutic approache
Externí odkaz:
https://doaj.org/article/64752bdb84f74e63a46333837d1bcd6a
Autor:
Wai W. Cheung, Wei Ding, Hal M. Hoffman, Zhen Wang, Sheng Hao, Ronghao Zheng, Alex Gonzalez, Jian-Ying Zhan, Ping Zhou, Shiping Li, Mary C. Esparza, Richard L. Lieber, Robert H. Mak
Publikováno v:
Scientific Reports, Vol 10, Iss 1, Pp 1-15 (2020)
Abstract Patients with chronic kidney disease (CKD) are often 25(OH)D3 and 1,25(OH)2D3 insufficient. We studied whether vitamin D repletion could correct aberrant adipose tissue and muscle metabolism in a mouse model of CKD-associated cachexia. Intra
Externí odkaz:
https://doaj.org/article/c7f89d5c634042d6a54496a2da92b2bc
Autor:
Wai W. Cheung, Sheng Hao, Zhen Wang, Wei Ding, Ronghao Zheng, Alex Gonzalez, Jian‐Ying Zhan, Ping Zhou, Shiping Li, Mary C. Esparza, Hal M. Hoffman, Richard L. Lieber, Robert H. Mak
Publikováno v:
Journal of Cachexia, Sarcopenia and Muscle, Vol 11, Iss 1, Pp 120-134 (2020)
Abstract Background Ctns−/− mice, a mouse model of infantile nephropathic cystinosis, exhibit hypermetabolism with adipose tissue browning and profound muscle wasting. Ctns−/− mice are 25(OH)D3 and 1,25(OH)2D3 insufficient. We investigated wh
Externí odkaz:
https://doaj.org/article/31642cf0eb224732ab914382a34923a3
Publikováno v:
International Journal of Molecular Sciences, Vol 23, Iss 23, p 15310 (2022)
Cachexia associated with chronic kidney disease (CKD) has been linked to GH resistance. In CKD, GH treatment enhances muscular performance. We investigated the impact of GH on cachexia brought on by CKD. CKD was induced by 5/6 nephrectomy in c57BL/6J
Externí odkaz:
https://doaj.org/article/93441412be1f4e9cbfc776d5d634a3ae
Publikováno v:
Cells, Vol 11, Iss 20, p 3264 (2022)
Manifestations of infantile nephropathic cystinosis (INC) often include cachexia and deficiency of circulating vitamin D metabolites. We examined the impact of 25(OH)D3 versus 1,25(OH)2D3 repletion in Ctns null mice, a mouse model of INC. Six weeks o
Externí odkaz:
https://doaj.org/article/ab244ab7fc2644f0b6f157e0bb0a2565
Publikováno v:
Cells, Vol 10, Iss 12, p 3382 (2021)
Patients with chronic kidney disease (CKD) often have low serum concentrations of 25(OH)D3 and 1,25(OH)2D3. We investigated the differential effects of 25(OH)D3 versus 1,25(OH)2D3 repletion in mice with surgically induced CKD. Intraperitoneal supplem
Externí odkaz:
https://doaj.org/article/330dacbec3e9456689ad8dbcce386858
Autor:
Alex Gonzalez, Wai W. Cheung, Elliot A. Perens, Eduardo A. Oliveira, Arieh Gertler, Robert H. Mak
Publikováno v:
Cells, Vol 10, Iss 8, p 1954 (2021)
Mice lacking the functional cystinosin gene (Ctns−/−), a model of infantile nephropathic cystinosis (INC), exhibit the cachexia phenotype with adipose tissue browning and muscle wasting. Elevated leptin signaling is an important cause of chronic
Externí odkaz:
https://doaj.org/article/a4cc77c8fd974a599721a1d9e4a8bc88