Small molecule STING inhibition improves myocardial infarction remodeling
Lavinia Rech; Mahmoud Abdellatif; Maria Pöttler; Verena Stangl; Nishani S. Mabotuwana; Sean A. Hardy; Peter P. Rainer · 2021 · Life Sciences
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
AIMS: Myocardial infarction (MI) is a major global cause of death. Massive cell death leads to inflammation, which is necessary for ensuing wound healing. Extensive inflammation, however, promotes infarct expansion and adverse remodeling. The DNA sensing receptor cyclic GMP-AMP synthase and its downstream signaling effector stimulator of interferon genes (cGAS-STING) is central in innate immune reactions in infections or autoimmunity. Cytosolic double-strand DNA activates the pathway and down-stream inflammatory responses. Recent papers demonstrated that this pathway is also active following M
Abstract by Lavinia Rech; Mahmoud Abdellatif; Maria Pöttler; Verena Stangl; Nishani S. Mabotuwana; Sean A. Hardy; Peter P. Rainer, Life Sciences (2021) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1016/j.lfs.2021.120263