bims-lypmec 2024-09-15 papers

Issue of 2024‒09‒15
four papers selected by
Satoru Kobayashi, New York Institute of Technology

Int J Mol Sci. 2024 Aug 31. pii: 9481. [Epub ahead of print]25(17):

Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue.

Antonella Galeone, Alessia Annicchiarico, Cinzia Buccoliero, Barbara Barile, Giovanni Battista Luciani, Francesco Onorati, Grazia Paola Nicchia, Giacomina Brunetti.

Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development.

Keywords: apoptosis; autophagy; diabetic cardiomyopathy; exosomes; ferroptosis; fibrosis; pyroptosis

DOI: https://doi.org/10.3390/ijms25179481

J Cell Biol. 2024 Oct 07. pii: e202407194. [Epub ahead of print]223(10):

A new player in the biogenesis of lysosome-related organelles.

Anbing Shi.

How are Rab GTPases regulated during lysosome-related organelle (LRO) biogenesis? Li et al. (https://doi.org/10.1083/jcb.202402016) identify LYSMD proteins as crucial activators of Rab32-family GTPases in LRO development, shedding light on the previously ambiguous mechanisms governing Rab functionality in this process.

DOI: https://doi.org/10.1083/jcb.202407194

Curr Heart Fail Rep. 2024 Sep 07.

Metabolic Adaptation in Heart Failure and the Role of Ketone Bodies as Biomarkers.

Michael W Foster, Joshua M Riley, Praneet C Kaki, Amine Al Soueidy, Ehson Aligholiazadeh, J Eduardo Rame.

PURPOSE OF REVIEW: The development and progression of heart failure is characterized by metabolic and physiologic adaptations allowing patients to cope with cardiac insufficiency. This review explores the changes in metabolism in heart failure and the potential role of biomarkers, particularly ketone bodies, in staging and prognosticating heart failure progression.RECENT FINDINGS: Recent insights into myocardial metabolism shed light on the heart's response to stress, highlighting the shift towards reliance on ketone bodies as an alternative fuel source. Elevated blood ketone levels have been shown to correlate with the severity of cardiac dysfunction, emphasizing their potential as prognostic indicators. Furthermore, studies exploring therapeutic interventions targeting specific metabolic pathways offer promise for improving outcomes in heart failure. Ketones have prognostic utility in heart failure, and potentially, an avenue for therapeutic intervention. Challenges remain in deciphering the optimal balance between metabolic support and exacerbating cardiac remodeling. Future research endeavors must address these complexities to advance personalized approaches in managing heart failure.

Keywords: Biomarkers; Cardiomyopathy; Heart failure; Ketone bodies; Myocardial metabolism

DOI: https://doi.org/10.1007/s11897-024-00678-6

STAR Protoc. 2024 Sep 12. pii: S2666-1667(24)00474-X. [Epub ahead of print]5(3): 103309

Protocol for detecting lysosome quantity and membrane permeability in acute myeloid leukemia cell lines.

Kexiu Huang, Xinya Jiang, Juan Du, Hui Zeng.

Lysosomal function and activity are essential to support cellular adaptation to multiple stresses. For example, certain drugs can induce increased lysosomal membrane permeability to exert their anti-cancer effects. Here, we present a protocol to evaluate the lysosome alterations induced by drug treatment. We first describe the steps for inducing lysosomal alterations in cultured cells. We then show how to quantify the number of lysosomes, assess the integrity of lysosomal membranes, and determine lysosomal membrane permeabilization by using galectin puncta assay. For complete details on the use and execution of this protocol, please refer to Jiang et al.1.

Keywords: cancer; cell biology; cell culture; flow cytometry

DOI: https://doi.org/10.1016/j.xpro.2024.103309