Results 41 to 50 of about 10,805 (242)

Septic Cardiomyopathy Mimicking Myocarditis or Inherited Cardiomyopathy

open access: yesJournal of Cardiovascular Magnetic Resonance
Yousef Daryani, MD, PhD   +1 more
doaj   +2 more sources

Targeted decrease of portal hepatic pressure gradient improves ascites control after TIPS

open access: yesHepatology, EarlyView., 2022
The river diagram demonstrates that after transjugular intrahepatic portosystemic shunt insertion (TIPS) the majority of patients without ascites and 50% of the patients with ascites detectable at ultrasound, show the best response in the long term follow‐up.
Alexander Queck   +14 more
wiley   +1 more source

G3BP1 Succinylation at K413 is Critical for Cardiac Function by Modulating PI3K‐AKT‐mTOR Signal Axis

open access: yesAdvanced Science, EarlyView.
Schematic illustrating the impact of G3BP1 succinylation at K413 on cardiac function. In the healthy human heart, G3BP1 succinylation maintains homeostatic mTOR signaling. In patients with dilated cardiomyopathy (DCM) and heart failure (HF), G3BP1 de‐succinylation induces RagA expression and disrupts the binding of the TSC1/2 complex, leading to the ...
Yuan Zhang   +9 more
wiley   +1 more source

Inhibition of the NLRP3/IL‐1β axis protects against sepsis‐induced cardiomyopathy

open access: yesJournal of Cachexia, Sarcopenia and Muscle, 2021
Background Septic cardiomyopathy worsens the prognosis of critically ill patients. Clinical data suggest that interleukin‐1β (IL‐1β), activated by the NLRP3 inflammasome, compromises cardiac function.
Katharina Busch   +20 more
doaj   +1 more source

Cardiac-specific ITCH overexpression ameliorates septic cardiomyopathy via inhibition of the NF-κB signaling pathway

open access: yesJournal of Molecular and Cellular Cardiology Plus, 2022
Background: Septic cardiomyopathy is a common complication of septic shock and organ dysfunction. ITCH is a HECT (homologous to the E6-AP carboxyl-terminus)-type ubiquitin E3 ligase that plays a critical role in inflammatory suppression.
Yuji Saito   +15 more
doaj   +1 more source

Engineering Approaches to Modify Immunomodulatory Functions of Mesenchymal Stromal Cells (MSCs): Tissue Regeneration and Clinical Application

open access: yesAdvanced Science, EarlyView.
Mesenchymal stromal cells (MSCs) show promise for treating immune‐related disorders through immunomodulation and tissue regeneration. This review gives a brief overview of current clinical approval of MSC therapies. It also discussed how bioengineering, including genetic modification, biomaterial delivery, extracellular vesicles, and iPSC‐derived MSCs,
Sichen Yang   +6 more
wiley   +1 more source

The E3 Ligase RNF115 Aggravates Pathological Cardiac Hypertrophy via Ubiquitin‐Mediated Degradation of SPTBN1

open access: yesAdvanced Science, EarlyView.
In response to hypertrophic stimuli, increased c‑JUN phosphorylation upregulates RNF115, leading to SPTBN1 ubiquitination and degradation. which promotes F‑actin depolymerization and YAP activation, driving cardiac hypertrophy. The RNF115 inhibitor DTD effectively suppresses SPTBN1 ubiquitination and cardiac hypertrophy.
Yan Zu   +12 more
wiley   +1 more source

Progress of heparanase in septic cardiomyopathy: A review. [PDF]

open access: yesMedicine (Baltimore)
Septic cardiomyopathy (SCM) is a severe complication caused by sepsis, resulting in a high mortality rate. The current understanding of the pathogenic mechanism of SCM primarily involves endocardial injury, microcirculation disturbance, mitochondrial dysfunction and fibrosis.
Chen D   +5 more
europepmc   +3 more sources

The 9th International RASopathies Symposium

open access: yesAmerican Journal of Medical Genetics Part A, EarlyView.
ABSTRACT The RASopathies are a group of congenital disorders with overlapping clinical manifestations that are caused by pathogenic germline or early somatic variants that result in the hyperactivation of the RAS/mitogen‐activated protein kinase (MAPK) signaling pathway.
Pau Castel   +41 more
wiley   +1 more source

Expanding the Phenotype of TUFM‐Related Combined Oxidative Phosphorylation Deficiency 4

open access: yesAmerican Journal of Medical Genetics Part A, EarlyView.
ABSTRACT Combined oxidative phosphorylation deficiency 4 (COXPD4) is a rare mitochondrial condition caused by biallelic deleterious variants in the nuclear‐encoded gene TUFM. To date, most individuals with COXPD4 have presented with encephalopathy, hypotonia, and abnormal brain imaging. Many of the reported individuals died in infancy. We aim to expand
Noémie Villeneuve‐Cloutier   +2 more
wiley   +1 more source

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