MiR-1180 promotes cardiomyocyte cell cycle re-entry after injury through the NKIRAS2–NFκB pathway
Why is this work in the frame?
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.
Post-publication record
OpenAlex flags this work as retracted, but it carries no matching Retraction Watch record in this frame.
Abstract
Heart failure (HF) is associated with a considerable number of symptoms and significantly impaired health for humans, including reduced quality of life and physical functioning. Previous studies have indicated that miRNAs have important roles in regulating the development of HF. MiR-1180 is involved in the proliferation, migration, invasiveness, and chemoresistance of cancer cells; however, the underlying mechanisms and role of miR-1180 in the functioning of cardiomyocytes remains unclear. In this study, we found that miR-1180 promotes cell activity and cell cycle processes by driving energy generation through NKIRAS2, which declines over time during development. The expression of miR-1180 is down-regulated in cells subjected to hypoxia-reoxygenation, and use of an miR-1180 mimic significantly reduced myocardial injury and cell apoptosis. In addition, miR-1180 regulates the NFκB pathway through NKIRAS2 in cardiomyocytes. These findings suggest that miR-1180 maybe a novel therapeutic target for use in getting cardiomyocytes to re-enter the cell cycle as well as for cardiac repair following myocardial injury.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
The record
- Venue
- Biochemistry and Cell Biology
- Topic
- Cardiac Ischemia and Reperfusion
- Field
- Medicine
- Canadian institutions
- —
- Funders
- —
- Keywords
- Cell biologyCell cycleCell injuryChemistryCellBiologyApoptosisBiochemistry
- Has abstract in OpenAlex
- yes