Results 81 to 90 of about 132,920 (293)

Rapamycin Alleviates Heart Failure Caused by Mitochondrial Dysfunction and SERCA Hypoactivity in Syntaxin 12/13 Deficient Models

open access: yesAdvanced Science, EarlyView.
Rapamycin alleviates heart failure via TFEB and CaMKII pathways in Syntaxin 12/13 deficient models. Stx12 deficiency causes heart failure via impaired iron trafficking to mitochondria, reducing respiratory complexes and sarcoplasmic reticulum Ca2+‐ATPase (SERCA).
Run‐Zhou Yang   +12 more
wiley   +1 more source

LncRNA Foxo6os as a Novel “ Scaffold” Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure

open access: yesAdvanced Science, EarlyView.
Schematic overview showing that forkhead box O6, opposite strand (Foxo6os) acts as a “scaffold”, directly binding myosin‐binding protein‐C (MYBPC3) and recruiting protein kinase C (PKC‐α) to mediate site‐specific phosphorylation of MYBPC3. This post‐translational modification supports cardiac contraction by regulating L‐type Ca2+ channels, especially ...
Jie Sheng   +9 more
wiley   +1 more source

Parvalbumin affects skeletal muscle trophism through modulation of mitochondrial calcium uptake

open access: yesCell Reports, 2021
Summary: Parvalbumin (PV) is a cytosolic Ca2+-binding protein highly expressed in fast skeletal muscle, contributing to an increased relaxation rate. Moreover, PV is an “atrogene” downregulated in most muscle atrophy conditions.
Gaia Butera   +8 more
doaj  

Atrial Fibroblasts‐Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis

open access: yesAdvanced Science, EarlyView.
Exosome miR‐224‐5p derived from angiotensin II‐treated atrial fibroblasts creates a substrate for AF by promoting atrial electrical remodeling. Increased exosome miR‐224‐5p enhances AF susceptibility by inhibiting CACNA1c expression and decreasing ICa current of atrial cardiomyocytes.
Yue Yuan   +13 more
wiley   +1 more source

FOXM1 Protects Against Myocardial Ischemia‐Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1‐Dependent LKB1 Ubiquitination

open access: yesAdvanced Science, EarlyView.
FOXM1 maintains mitochondrial bioenergetic function by inhibiting MKRN1‐mediated ubiquitination of LKB1 in cardiomyocytes. Loss of FOXM1 in cardiomyocytes results in upregulation of MKRN1, which enhances LKB1 ubiquitination and disrupts AMPK signaling and energy metabolism pathways. Conversely, FOXM1 overexpression preserves mitochondrial bioenergetics
Shuai Song   +17 more
wiley   +1 more source

Modified hybrid training and neuromuscular electrical stimulation increase quadriceps femoral and hamstrings muscle hypertrophy in untrained healthy subjects

open access: yesRetos: Nuevas Tendencias en Educación Física, Deportes y Recreación
Purpose: Low physical activity leads to muscle atrophy due to lack of exercise time and sport facilities. Addressing this issue, there are alternative methods with shorter training time and less equipment to induce muscle hypertrophy which are ...
Johanna Chrestella   +5 more
doaj   +1 more source

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