The potential roles of stress-induced phosphoprotein 1 and connexin 43 in rats with reperfusion arrhythmia

Review Biochemistry & Molecular Biology

Ubiquitination in the regulation of inflammatory cell death and cancer

Peter E. Cockram et al.

Summary: The ubiquitin system is crucial for the modulation of cellular processes, including programmed cell death and inflammation. It controls protein degradation, cellular processes, and plays a key role in various diseases such as cancer.

CELL DEATH AND DIFFERENTIATION (2021)

添加到收藏夹

Review Biochemistry & Molecular Biology

The Hsp70-Hsp90 go-between Hop/Stip1/Sti1 is a proteostatic switch and may be a drug target in cancer and neurodegeneration

Kaushik Bhattacharya et al.

Summary: The Hsp70 and Hsp90 molecular chaperone systems in eukaryotes are crucial for protein homeostasis under normal and stressed conditions, exhibiting both physical and functional interactions to maintain cellular proteostasis. Co-chaperones like Hop and Sti1 play a key role in facilitating substrate transfer from Hsp70 to Hsp90. Interestingly, while eukaryotes rely on the canonical Hsp70-Hop-Hsp90 ternary chaperone complex for optimal maturation and stability of specific clients, prokaryotes can form a binary chaperone complex without Hop, displaying enhanced protein folding and anti-aggregation activities.

CELLULAR AND MOLECULAR LIFE SCIENCES (2021)

添加到收藏夹

Article Cell Biology

Stress-induced phosphoprotein 1 restrains spinal cord ischaemia-reperfusion injury by modulating NE-κB signalling

Hongdou Jin et al.

Summary: The study demonstrated that STIP1 alleviates neuronal injury and inflammation caused by spinal cord ischaemia/reperfusion by deactivating the NE-kappa B signaling pathway, suggesting potential insights for clinical diagnosis and treatment of SCI.

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2021)

添加到收藏夹

Article Chemistry, Multidisciplinary

Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43

Jia-dan Wang et al.

Summary: In this study, we elucidated the mechanisms of mitochondrial damage in ESC-CMs after knockdown of Rictor using a model of cardiomyocyte differentiation from mouse ES cells. Knockdown of Rictor led to swollen and ruptured mitochondria, decreased ATP production and mitochondrial transmembrane potential, inhibited mitochondrial respiratory chain complex activities, and hindered Cx43 translocation into mitochondria, ultimately resulted in mitochondrial dysfunction in ESC-CMs.

ACTA PHARMACOLOGICA SINICA (2021)

添加到收藏夹

Article Chemistry, Medicinal

Omacor Protects Normotensive and Hypertensive Rats Exposed to Continuous Light from Increased Risk to Malignant Cardiac Arrhythmias

Tamara Egan Benova et al.

Summary: The study found that continuous light exposure can lead to impaired intercellular electrical communication in rat hearts, increasing the risk of malignant arrhythmias. However, treatment with Omacor(R) can alleviate these adverse effects.

MARINE DRUGS (2021)

添加到收藏夹

Review Biochemistry & Molecular Biology

Mechanisms Underlying Connexin Hemichannel Activation in Disease

Raf Van Campenhout et al.

Summary: Gap junctions and connexin hemichannels play different roles in intercellular and extracellular communication, with the former maintaining homeostasis and the latter being associated with the onset and spread of disease by mediating messenger transport that fuels inflammation and cell death in various diseases. The present review discusses the mechanisms involved in the activation of connexin hemichannels during pathology.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2021)

添加到收藏夹

Article Medicine, Research & Experimental

Cx43 hemichannel microdomain signaling at the intercalated disc enhances cardiac excitability

Maarten A. J. De Smet et al.

Summary: Cx43 hemichannels are activated during diastolic Ca2+ release in ventricular cardiomyocytes, contributing to enhanced Ca2+ dynamics due to Ca2+ entry and coupling to release microdomains. Hemichannel opening also leads to delayed afterdepolarizations and triggered action potentials. Increased hemichannel activity is associated with electrical instability in failing human hearts compared to nonfailing donor hearts, suggesting a potentially novel mechanism of cardiac arrhythmogenesis in heart failure.

JOURNAL OF CLINICAL INVESTIGATION (2021)

添加到收藏夹

Article Cardiac & Cardiovascular Systems

Rotigaptide Infusion for the First 7 Days After Myocardial Infarction-Reperfusion Reduced Late Complexity of Myocardial Architecture of the Healing Border-Zone and Arrhythmia Inducibility

Rasheda A. Chowdhury et al.

Summary: Enhancement of gap junctions function by rotigaptide during the early healing phase in reperfused infarction reduces later complexity of infarct scar morphology and programmed electrical stimulation-induced arrhythmias, suggesting it as a feasible intervention in the management of acute myocardial infarction to reduce late arrhythmic risk.

JOURNAL OF THE AMERICAN HEART ASSOCIATION (2021)

添加到收藏夹

Editorial Material Cell Biology

Opening the floodgates: An emerging role for Connexin-43 hemichannels in the heart

Mauricio A. Lillo et al.

CELL CALCIUM (2021)

添加到收藏夹

Article Biochemistry & Molecular Biology

Connexin 43 and Connexin 26 Involvement in the Ponatinib-Induced Cardiomyopathy: Sex-Related Differences in a Murine Model

Rosalinda Madonna et al.

Summary: Cardiac connexins play a crucial role in proper heart function by mediating electrical and chemical signaling. This study found that female mice are less affected by ponatinib-induced cardiac toxicity compared to males, indicating potential sex-specific adaptative responses.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2021)

添加到收藏夹

Article Physiology

Quantitative Proteomics Reveal That Metabolic Improvement Contributes to the Cardioprotective Effect of T89 on Isoproterenol-Induced Cardiac Injury

Xiao-Hong Wei et al.

Summary: This study demonstrated that T-89 has a significant protective effect on ISO-induced cardiac injury by regulating glycolipid metabolism and restoring mitochondrial function. Additionally, T-89 can inhibit the phosphorylation of HSPs and ERK, protecting the heart from hypertrophy.

FRONTIERS IN PHYSIOLOGY (2021)

添加到收藏夹

Review Biochemistry & Molecular Biology