Phospholipid remodeling of the cardiomyocyte membrane affects cardiac function - Nature

AcknowledgementsWe thank Yukiko Banzai, Yuko Ishiyama, Asami Ogawa, and Yingda Xiao of the University of Tokyo for their assistance with animal experiments and laboratory work. We are grateful to Yuriko Sakamaki of the Ochanomizu Research Facility, Institute of Science Tokyo, for her technical support with electron microscopy sample preparation and imaging. FundingThis work was supported by Grants-in-Aid for Scientific Research, Japan [grant Nos. 24K19023 to S. B. and 22K08174 to H. T.]; Sakakibara Heart Foundation Cardiovascular Research Program 2023 (to S. B.); Japan Foundation for Applied Enzymology (to S. B.). I. K. was supported by a Grant-in-Aid for Scientific Research (S) of the Japan Society for the Promotion of Science and by the Japan Agency for Medical Research, Development (JP20ek0210152, JP18gm6210010, JP20ek0210141, JP20ek0109440, JP20ek0109487, JP17gm0810013, JP18km0405209, JP21ek0109543, JP21ek0109569, JP21tm0724601, JP22ama121016, JP22ek0210172, JP22ek0210167, JP22bm1123011). Author informationAuthor notesThese authors contributed equally: Satoshi Bujo, Takayuki Fujiwara, Masayuki Kubota.

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply. AbstractCryptococcus neoformans and Cryptococcus gattii are fungal pathogens that cause life-threatening infections, including cryptococcal meningitis. A distinctive feature of the cryptococcal cell wall is the extensive deacetylation of chitin to chitosan, a modification that is essential for virulence but whose structural role in cell-wall organization remains poorly understood. Here, we analyze the cell walls of wild-type strains of both species and their avirulent chitosan-deficient mutants, which serve as vaccine candidates. Loss of chitosan disrupted cell morphology and altered cell-wall ultrastructure, with more pronounced defects in C. neoformans. Solid-state NMR reveals that aggregated α-(1→3)-glucans form the principal rigid domain of the cell wall in both species and are closely associated with chitin microfibrils, whereas surrounding β-glucans and mannoproteins constitute a more dynamic matrix.

Each time you eat a juicy pomegranate, your gut bacteria can produce a natural metabolite called urolithin A. This little-known compound is making a big splash. In recent years, scientists have paid close attention to urolithin A because it seems to have anti-inflammatory, antioxidant, anti-tumor, and anti-aging properties. Initial evidence in humans even suggests that urolithin A can help the body remove aged or damaged parts of our cells, thereby improving their overall health. Now, for the first time, researchers at King's College London (KCL) have found evidence that urolithin A can activate a protein that plays a key role in heart health. In mouse models with stiff and failing hearts, urolithin A improved measures of heart function by as much as 80 percent compared to untreated animals, according to a press release from KCL. The findings are published in Science Advances, with financial support from the British Heart Foundation. The results have scientists hopeful that urolithin A could be a previously unidentified treatment option for a common form of heart failure.

Yunduan Wang1 na1, Shaohui Beng1 na1, Kechao Chen1 na1, Xiaowei Li2, Shuang Zhang1, Xiaoqiang He2, Yunqiang Jia2, Yanwen Wang2, Yuhan Xiang1, Yan Xiong1,3, Daoliang Lan1,3, Jian Li1,3 & … Wei Fu1,3 We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.