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Tatiana Kisseleva

Researcher at University of California, San Diego

Publications -  130
Citations -  13403

Tatiana Kisseleva is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Hepatic stellate cell & Fibrosis. The author has an hindex of 48, co-authored 110 publications receiving 9901 citations. Previous affiliations of Tatiana Kisseleva include Columbia University & University of Southern California.

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Signaling through the JAK/STAT pathway, recent advances and future challenges.

TL;DR: Significant progress has been made in the characterization of the JAK/STAT signaling cascade, including the identification of multiple STATs and regulatory proteins, and the solution of the crystal structure of two STATs has and will continue to facilitate the understanding of how STATs function.
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Pericytes and perivascular fibroblasts are the primary source of collagen-producing cells in obstructive fibrosis of the kidney.

TL;DR: These results serve to refocus fibrosis research to injury of the vasculature rather than injury to the epithelium, and suggest that either vascular injury or vascular factors are the most likely triggers for pericyte migration and differentiation into myofibroblasts.
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Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis

TL;DR: It is demonstrated that half of the myofibroblasts escape apoptosis during regression of liver fibrosis, down-regulate fibrogenic genes, and acquire a phenotype similar to, but distinct from, quiescent HSCs in their ability to more rapidly reactivate into my ofibro Blasts in response to fibrogened stimuli.
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New mitochondrial DNA synthesis enables NLRP3 inflammasome activation

TL;DR: It is shown that the synthesis of mitochondrial DNA (mtDNA), induced after the engagement of Toll-like receptors, is crucial for NLRP3 signalling, and the dependence on CMPK2 catalytic activity provides opportunities for more effective control ofNLRP3 inflammasome-associated diseases.
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Molecular and cellular mechanisms of liver fibrosis and its regression.

TL;DR: This Review summarizes studies of the molecular mechanisms underlying the reversibility of liver fibrosis, including apoptosis and the inactivation of hepatic stellate cells, the crosstalk between the liver and the systems that orchestrate the recruitment of bone marrow-derived macrophages driving fibrosis resolution, and the interactions between various cell types that lead to the intracellular signalling that induces fibrosis or its regression.