Results 141 to 150 of about 863,016 (307)

SerpinA3 is an Endogenous TGF‐β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling

open access: yesAdvanced Science, EarlyView.
SerpinA3 acts as an endogenous TGF‐β receptor antagonist that binds to the extracellular domain of TGFR‐1, thereby preventing TGFR‐1–TGFR‐2 complex formation. This receptor‐level blockade suppresses TGF‐β/Smad2/3 signaling, attenuates cardiac fibroblast activation, and extracellular matrix deposition, and ultimately alleviates pressure overload–induced
Hui Wang   +9 more
wiley   +1 more source

The management of myocardial infarction

open access: yes, 2019
This thesis describes the causes, risk factors and patho-anatomical changes that occur during myocardial infarction. The accompanying signs and symptoms, as well as the diagnosis and ECG changes.
Okuns, Aaron
core  

An RNA‐Binding Protein RBMS1 Promotes Endothelial Cell Autophagy to Maintain Vascular Homeostasis and Suppress Deep Vein Thrombosis

open access: yesAdvanced Science, EarlyView.
RBMS1, an RNA‐binding protein, restores vascular endothelial homeostasis by enhancing ATG3‐mediated autophagy, thereby attenuating thrombus formation and suggesting a potential avenue for further therapeutic exploration in DVT. ABSTRACT Deep vein thrombosis (DVT) is a prevalent vascular disorder characterized by aberrant coagulation within the deep ...
Chu Chu   +13 more
wiley   +1 more source

Identification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities

open access: yesNature Communications
Genomics can provide insight into the etiology of type 2 diabetes and its comorbidities, but assigning functionality to non-coding variants remains challenging.
Douglas P. Loesch   +20 more
doaj   +1 more source

Macrophage PARP7 Alleviates Septic Cardiomyopathy by Interacting With TBK1 and Suppressing TBK1‐Driven Inflammatory Response

open access: yesAdvanced Science, EarlyView.
In septic cardiomyopathy, PARP7 directly binds TBK1 and mediates its ADP‐ribosylation, thereby repressing TBK1‐driven proinflammatory signaling in macrophages. ABSTRACT Septic cardiomyopathy is a life‐threatening complication of sepsis, and an uncontrolled inflammatory response represents a key pathogenic mechanism. PARP7 negatively regulates the IFN‐I
Jibo Han   +10 more
wiley   +1 more source

Research Advances in Myocardial Infarction Repair and Cardiac Regenerative Medicine via the Notch Signaling Pathway

open access: yesReviews in Cardiovascular Medicine
Acute myocardial infarction is myocardial necrosis caused by acute and persistent ischemia and hypoxia in the coronary artery and severely affects public health.
Songyan Cai, Qingyuan Dai
doaj   +1 more source

THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A

open access: yesAdvanced Science, EarlyView.
THSD7A exerts pro‐inflammatory effects and exacerbates atherosclerosis. Mechanistically, THSD7A regulates endothelial cell inflammation and atherosclerosis by activating the αvβ3/CEBPD/IL1A signaling axis. THSD7A is not only a genetic marker but also a potential therapeutic target for coronary artery disease (CAD).
Jiankun Liu   +15 more
wiley   +1 more source

CAR‐Engineered Cell Therapies Beyond Cancer: Reprogramming Fibrosis and Immune‐Mediated Inflammation

open access: yesAdvanced Science, EarlyView.
CAR‐engineered cell therapies are expanding beyond cancer toward immune resetting, pathological‐cell clearance, matrix remodeling, and microenvironmental reprogramming in autoimmune, inflammatory, and fibrotic diseases. This Review compares CAR‐T, CAR‐macrophage, and CAR‐NK platforms and proposes controllable spatiotemporal reprogramming to align ...
Peng Jun Xu   +6 more
wiley   +1 more source

The effect of carvacrol on kidney injury caused by isopreterenol-induced myocardial infarction

open access: yesBMC Nephrology
Background Myocardial infarction is a major cause of morbidity and mortality, often leading to heart and kidney dysfunction. Despite advancements in treatment, the link between heart and kidney damage is poorly understood. This study aims to evaluate the
Gülhan Ünlü   +2 more
doaj   +1 more source

Periostin‐CCL3 Feedforward Signaling Loop Promotes Cardiac Fibrosis and Cardiomyocyte Necroptosis in Arrhythmogenic Cardiomyopathy

open access: yesAdvanced Science, EarlyView.
POSTN‐CCL3 signaling forms a feed‐forward circuit between cardiomyocytes and cardiac myofibroblasts in arrhythmogenic cardiomyopathy. POSTN activates JNK/RIP3‐dependent necroptotic signaling and JNK/ETS2‐induced CCL3 expression in cardiomyocytes. In turn, CCL3‐CCR5 signaling in cardiac myofibroblasts activates NF‐κB/p65 and promotes POSTN expression ...
Tiantian Wu   +12 more
wiley   +1 more source

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