-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Currently, acute ischemic stroke can be treated by using recombinant tissue plasminogen activator (rtPA) intravenous thrombolysis and/or mechanical thrombectomy
.
Although both methods are effective, they also have limitations
.
Currently, acute ischemic stroke can be treated by using recombinant tissue plasminogen activator (rtPA) intravenous thrombolysis and/or mechanical thrombectomy
Recently, a research team found that in humans and mice, after an ischemic stroke, the nuclear pyruvate kinase muscle 2 (PKM2) in neutrophils is a modulator of systemic inflammation.
They used existing comorbidities.
Recently, a research team found that in humans and mice, after an ischemic stroke, the nuclear pyruvate kinase muscle 2 (PKM2) in neutrophils is a modulator of systemic inflammation.
A new type of bone marrow cell-specific PKM2 -/- mice were generated on wild-type (PKM2fl/flLysMCre) and hyperlipidemia background (PKM2fl/flLysMCre Apoe-/-)
The genetic deletion of PKM2 in bone marrow cells limits the inflammatory response of peripheral neutrophils after cerebral ischemia/reperfusion, and reduces the extracellular traps of neutrophils, which indicates that PKM2 promotes neutrophil production during stroke.
In filamentous body and autologous clot/rtPA stroke models, regardless of gender, the loss of PKM2 in myeloid cells of wild-type or hyperlipidemia mice reduces infarction and enhances long-term sensorimotor recovery
Mechanismally, PKM2 regulates the inflammation of peripheral neutrophils after ischemia by promoting the phosphorylation of STAT3
Overall, these findings indicate that PKM2 is a new therapeutic target that can improve brain salvage and recovery after reperfusion
Original source:
Nirav Dhanesha, Rakesh B.
Patel, Prakash Doddapattar, Madankumar Ghatge, Gagan D Flora, Manish Jain, Daniel Thedens, Heena Olalde, Mariia Kumskova, Enrique Leira, Anil K Chauhan; PKM2 promotes neutro activation and cerebral thrombo-inflammation: Therapeutic implications: ischemic stroke .
Nirav Dhanesha, Rakesh B.
Patel, Prakash Doddapattar, Madankumar Ghatge, Gagan D Flora, Manish Jain, Daniel Thedens, Heena Olalde, Mariia Kumskova, Enrique Leira, Anil K Chauhan; PKM2 promotes neutro activation and cerebral thrombo-inflammation: Therapeutic implications: ischemic stroke .
PKM2 promotes neutrophil activation and cerebral thrombo-inflammation: Therapeutic implications for ischemic stroke Blood Blood2021; blood.
2021012322.
doi:https://doi.
org/10.
1182/blood.
2021012322 Leave a message here