Results 91 to 100 of about 218,133 (348)

Chinese and western medicine treatment of myocardial fibrosis drugs

open access: yesFrontiers in Cardiovascular Medicine
Myocardial fibrosis (MF) is a common pathological manifestation of many cardiovascular diseases, such as myocardial infarction, myocardial ischemia, and sudden cardiac death.
Yuxi Zhu   +7 more
doaj   +1 more source

Cardiac hypertrophy and heart failure: from the case to review of literature [PDF]

open access: yes, 2016
In response to an increased workload due to physiological or pathological stimuli, the heart may undergo a process of growth with increased muscle mass called cardiac hypertrophy. It is a particular mechanism of long term compensation used by the heart
Massoni, Francesco   +4 more
core   +1 more source

Conformable Microelectrode Arrays Integrated with a Scoop‐Shaped Slide‐Well for Dynamic Electrophysiological Profiling of Patient‐Derived Cardiac Organoids

open access: yesAdvanced Science, EarlyView.
A flexible, ultrathin multi‐channel microelectrode array (MEA) conformally integrated onto a curved slide‐well enables stable electrical interfacing with 3D cardiac organoids. The geometry‐guided self‐alignment allows simultaneous recording of extracellular field potentials and contractile motion from irregular, beating tissues.
Ye Seul Kim   +12 more
wiley   +1 more source

Biomarkers Beyond the Natriuretic Peptides for Chronic Heart Failure: Galectin-3 and Soluble ST2. [PDF]

open access: yes, 2012
B-type natriuretic peptide (BNP) and NT-proBNP are widely used plasma biomarkers for the diagnosis of acute decompensated heart failure and prognosis for future cardiac disease.
Wu, Alan HB
core   +1 more source

Tissue Microenvironments Define and Get Reinforced by Macrophage Phenotypes in Homeostasis or during Inflammation, Repair and Fibrosis [PDF]

open access: yes, 2012
Current macrophage phenotype classifications are based on distinct in vitro culture conditions that do not adequately mirror complex tissue environments.
Weidenbusch, Marc, Anders, Hans-Joachim
core   +1 more source

Fibroblast Activation Protein Promotes Thoracic Aortic Dissection via PLAUR/ITGB1‐Mediated Pro‐inflammatory Macrophage Polarization

open access: yesAdvanced Science, EarlyView.
This study reveals that FAP promotes thoracic aortic dissection (TAD) through a nonenzymatic mechanism involving fibroblast‐macrophage crosstalk via the FAP/PLAUR/ITGB1/FAK axis. Targeting this pathway might offer a promising therapeutic strategy for TAD.
Hongqiao Zhu   +7 more
wiley   +1 more source

Non-coding RNAs: targets for Chinese herbal medicine in treating myocardial fibrosis

open access: yesFrontiers in Pharmacology
Cardiovascular diseases have become the leading cause of death in urban and rural areas. Myocardial fibrosis is a common pathological manifestation at the adaptive and repair stage of cardiovascular diseases, easily predisposing to cardiac death.
Minghui Wang   +12 more
doaj   +1 more source

Irgm1 Improves Postinfarction Cardiac Repair by Promoting Neutrophil Clearance and Efferocytosis

open access: yesAdvanced Science, EarlyView.
The Irgm1‐PDIA3 axis enhances post‐infarction cardiac repair by accelerating neutrophil clearance and facilitating efferocytosis. Irgm1 holds potential as a prognostic biomarker in MI, and LOC14 may represent a therapeutic option to improve cardiac repair, especially in cases of Irgm1 deficiency.
Zeng Wang   +14 more
wiley   +1 more source

Drug treatment of hypertension: focus on vascular health [PDF]

open access: yes, 2016
Hypertension, the most common preventable risk factor for cardiovascular disease and death, is a growing health burden. Serious cardiovascular complications result from target organ damage including cerebrovascular disease, heart failure, ischaemic heart
Cameron, Alan C.   +2 more
core   +1 more source

Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

open access: yesAdvanced Science, EarlyView.
The study demonstrated that connexin43 (Cx43) knockout caused arrhythmic phenotype and decreased proline content in vitro and in vivo. Mechanistically, Cx43 interacts with the amino acid transporter SNAT2 (sodium‐dependent neutral amino acid transporter), and its deficiency disrupts proline transport and metabolism.
Hangying Ying   +8 more
wiley   +1 more source

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