Mohammed Shakil Ahmed
- Senior scientist, PhD
- +47 23071407
Muhammad Shakil Ahmed received his MSc in Biotechnology and PhD in Molecular Cardiology from University of Oslo. His work focuses on molecular mechanisms of cardiopulmonary fibrosis.
Publications 2021
Instability in NAD(+) metabolism leads to impaired cardiac mitochondrial function and communication
eLife, 10, e59828
DOI 10.7554/eLife.59828
Hepatic connective tissue growth factor expression and regulation differ between non-steatotic and non-alcoholic steatotic livers from brain-dead donor
Sci Rep, 11 (1), 3857
DOI 10.1038/s41598-021-83516-2
Publications 2020
Absence of NLRP3 Inflammasome in Hematopoietic Cells Reduces Adverse Remodeling After Experimental Myocardial Infarction
JACC-Basic Transl. Sci., 5 (12), 1210-1224
DOI 10.1016/j.jacbts.2020.09.013
Exercise training reveals micro-RNAs associated with improved cardiac function and electrophysiology in rats with heart failure after myocardial infarction
J. Mol. Cell. Cardiol., 148, 106-119
DOI 10.1016/j.yjmcc.2020.08.015
Publications 2019
Low Cellular NAD(+) Compromises Lipopolysaccharide-Induced Inflammatory Responses via Inhibiting TLR4 Signal Transduction in Human Monocytes
J. Immunol., 203 (6), 1598-1608
DOI 10.4049/jimmunol.1801382
Publications 2017
N-Acetylcysteine Amide Exerts Possible Neuroprotective Effects in Newborn Pigs after Perinatal Asphyxia
Neonatology, 111 (1), 12-21
DOI 10.1159/000447255
Toll-Like Receptor 9 Promotes Survival in SERCA2a KO Heart Failure Mice
Mediat. Inflamm., 2017, 9450439
DOI 10.1155/2017/9450439
Publications 2016
CTGF/CCN2 Postconditioning Increases Tolerance of Murine Hearts towards Ischemia-Reperfusion Injury
PLoS One, 11 (2), e0149000
DOI 10.1371/journal.pone.0149000
Publications 2015
Sustained Toll-Like Receptor 9 Activation Promotes Systemic and Cardiac Inflammation, and Aggravates Diastolic Heart Failure in SERCA2a KO Mice
PLoS One, 10 (10), e0139715
DOI 10.1371/journal.pone.0139715
Publications 2013
CCN2/CTGF attenuates myocardial hypertrophy and cardiac dysfunction upon chronic pressure-overload
Int. J. Cardiol., 168 (3), 2049-2056
DOI 10.1016/j.ijcard.2013.01.165
CCN2 exerts direct cytoprotective actions in adult cardiac myocytes by activation of the PI3-kinase/Akt/GSK-3 beta signaling pathway
J. Cell Commun. Signal, 7 (1), 31-47
DOI 10.1007/s12079-012-0183-1
Publications 2012
Myocardial Connective Tissue Growth Factor (CCN2/CTGF) Attenuates Left Ventricular Remodeling after Myocardial Infarction
PLoS One, 7 (12), e52120
DOI 10.1371/journal.pone.0052120
Cardiomyocyte-restricted inhibition of G protein-coupled receptor kinase-3 attenuates cardiac dysfunction after chronic pressure overload
Am. J. Physiol.-Heart Circul. Physiol., 303 (1), H66-H74
DOI 10.1152/ajpheart.00724.2011
Publications 2011
Collagen isoform shift during the early phase of reverse left ventricular remodelling after relief of pressure overload
Eur. Heart J., 32 (2), 236-245
DOI 10.1093/eurheartj/ehq166
Publications 2010
Adrenomedullin is increased in alveolar macrophages and released from the lungs into the circulation in severe heart failure
Basic Res. Cardiol., 105 (1), 89-98
DOI 10.1007/s00395-009-0070-y
Activation of Notch signaling in cardiomyocytes during post-infarction remodeling
Scand. Cardiovasc. J., 44 (6), 359-366
DOI 10.3109/14017431.2010.511256
Publications 2007
Induction of pulmonary connective tissue growth factor in heart failure is associated with pulmonary parenchymal and vascular remodeling
Cardiovasc. Res., 74 (2), 323-333
DOI 10.1016/j.cardiores.2006.12.010
Substrate specificities of G protein-coupled receptor kinase-2 and -3 at cardiac myocyte receptors provide basis for distinct roles in regulation of myocardial function
Mol. Pharmacol., 72 (3), 582-591
DOI 10.1124/mol.107.035766