bims-lypmec Biomed News
on Lysosomal positioning and metabolism in cardiomyocytes
Issue of 2024‒08‒25
ten papers selected by
Satoru Kobayashi, New York Institute of Technology



  1. Elife. 2024 Aug 21. pii: e102430. [Epub ahead of print]13
      The formation of large endolysosomal structures in unfertilized eggs ensures that lysosomes remain dormant before fertilization, and then shift into clean-up mode after the egg-to-embryo transition.
    Keywords:  ELYSA; cell biology; developmental biology; embryo; endosome; fertilization; lysosome; mouse; oocyte
    DOI:  https://doi.org/10.7554/eLife.102430
  2. Nature. 2024 Aug 21.
      Mitochondrial membranes define distinct structural and functional compartments. Cristae of the inner mitochondrial membrane (IMM) function as independent bioenergetic units that undergo rapid and transient remodelling, but the significance of this compartmentalized organization is unknown1. Using super-resolution microscopy, here we show that cytosolic IMM vesicles, devoid of outer mitochondrial membrane or mitochondrial matrix, are formed during resting state. These vesicles derived from the IMM (VDIMs) are formed by IMM herniation through pores formed by voltage-dependent anion channel 1 in the outer mitochondrial membrane. Live-cell imaging showed that lysosomes in proximity to mitochondria engulfed the herniating IMM and, aided by the endosomal sorting complex required for transport machinery, led to the formation of VDIMs in a microautophagy-like process, sparing the remainder of the organelle. VDIM formation was enhanced in mitochondria undergoing oxidative stress, suggesting their potential role in maintenance of mitochondrial function. Furthermore, the formation of VDIMs required calcium release by the reactive oxygen species-activated, lysosomal calcium channel, transient receptor potential mucolipin 1, showing an interorganelle communication pathway for maintenance of mitochondrial homeostasis. Thus, IMM compartmentalization could allow for the selective removal of damaged IMM sections via VDIMs, which should protect mitochondria from localized injury. Our findings show a new pathway of intramitochondrial quality control.
    DOI:  https://doi.org/10.1038/s41586-024-07835-w
  3. Nature. 2024 Aug;632(8027): 987-988
      
    Keywords:  Biochemistry; Cell biology
    DOI:  https://doi.org/10.1038/d41586-024-02528-w
  4. Anal Chem. 2024 Aug 22.
      The mitochondria, as one of the essential organelles in cells, are closely associated with numerous biological processes. Therefore, the realization of clear and real-time imaging for tracking mitochondria is of profound significance. Here, we present a mitochondria-targeting fluorescent probe, N(CH2)3-PD-NEt, for the real-time fluorescence imaging of mitochondria in living cells. Using the probe, the fluorescence changes of mitochondria stimulated by different drugs were successfully observed by fluorescence imaging. In addition, the dynamic processes of mitochondria and lysosomes during apoptosis were also explored. Importantly, we observed several novel dynamic interaction patterns between mitochondria and lysosomes. Among them, the most prominent pattern involved the noncontact movements of two lysosomes, that is, one lysosome gradually approached the other lysosome over time, eventually coming into contact and merging with it while gradually combining with mitochondria to form new mitochondria. Notably, the protrusions of the mitochondria became increasingly evident during this process. Meanwhile, we successfully observed the dynamic changes of mitochondria with SIM super-resolution imaging. The study provides promising help for the in-depth study of the dynamic processes of mitochondrial physiology and pathology and the study of the interactions between organelles.
    DOI:  https://doi.org/10.1021/acs.analchem.4c03273
  5. Proc Natl Acad Sci U S A. 2024 Aug 27. 121(35): e2322755121
      The mechanistic target of rapamycin complex 1 (mTORC1) pathway regulates cell growth and metabolism in response to many environmental cues, including nutrients. Amino acids signal to mTORC1 by modulating the guanine nucleotide loading states of the heterodimeric Rag GTPases, which bind and recruit mTORC1 to the lysosomal surface, its site of activation. The Rag GTPases are tethered to the lysosome by the Ragulator complex and regulated by the GATOR1, GATOR2, and KICSTOR multiprotein complexes that localize to the lysosomal surface through an unknown mechanism(s). Here, we show that mTORC1 is completely insensitive to amino acids in cells lacking the Rag GTPases or the Ragulator component p18. Moreover, not only are the Rag GTPases and Ragulator required for amino acids to regulate mTORC1, they are also essential for the lysosomal recruitment of the GATOR1, GATOR2, and KICSTOR complexes, which stably associate and traffic to the lysosome as the "GATOR" supercomplex. The nucleotide state of RagA/B controls the lysosomal association of GATOR, in a fashion competitively antagonized by the N terminus of the amino acid transporter SLC38A9. Targeting of Ragulator to the surface of mitochondria is sufficient to relocalize the Rags and GATOR to this organelle, but not to enable the nutrient-regulated recruitment of mTORC1 to mitochondria. Thus, our results reveal that the Rag-Ragulator complex is the central organizer of the physical architecture of the mTORC1 nutrient-sensing pathway and underscore that mTORC1 activation requires signal transduction on the lysosomal surface.
    Keywords:  biochemistry; mTOR signaling; nutrient sensing
    DOI:  https://doi.org/10.1073/pnas.2322755121
  6. Front Cell Dev Biol. 2024 ;12 1431566
      Lysosomes serve as catabolic centers and signaling hubs in cells, regulating a multitude of cellular processes such as intracellular environment homeostasis, macromolecule degradation, intracellular vesicle trafficking and autophagy. Alterations in lysosomal level and function are crucial for cellular adaptation to external stimuli, with lysosome dysfunction being implicated in the pathogenesis of numerous diseases. Osteoclasts (OCs), as multinucleated cells responsible for bone resorption and maintaining bone homeostasis, have a complex relationship with lysosomes that is not fully understood. Dysregulated function of OCs can disrupt bone homeostasis leading to the development of various bone disorders. The regulation of OC differentiation and bone resorption for the treatment of bone disease have received considerable attention in recent years, yet the role and regulation of lysosomes in OCs, as well as the potential therapeutic implications of intervening in lysosomal biologic behavior for the treatment of bone diseases, remain relatively understudied. This review aims to elucidate the mechanisms involved in lysosomal biogenesis and to discuss the functions of lysosomes in OCs, specifically in relation to differentiation, bone resorption, and autophagy. Finally, we explore the potential therapeutic implication of targeting lysosomes in the treatment of bone metabolic disorders.
    Keywords:  autophagy; bone metabolic disorders; bone resorption; lysosome; osteoclast
    DOI:  https://doi.org/10.3389/fcell.2024.1431566
  7. Nat Cell Biol. 2024 Aug 22.
      Cells release intraluminal vesicles in multivesicular bodies as exosomes to communicate with other cells. Although recent studies suggest an intimate link between exosome biogenesis and autophagy, the detailed mechanism is not fully understood. Here we employed comprehensive RNA interference screening for autophagy-related factors and discovered that Rubicon, a negative regulator of autophagy, is essential for exosome release. Rubicon recruits WIPI2d to endosomes to promote exosome biogenesis. Interactome analysis of WIPI2d identified the ESCRT components that are required for intraluminal vesicle formation. Notably, we found that Rubicon is required for an age-dependent increase of exosome release in mice. In addition, small RNA sequencing of serum exosomes revealed that Rubicon determines the fate of exosomal microRNAs associated with cellular senescence and longevity pathways. Taken together, our current results suggest that the Rubicon-WIPI axis functions as a key regulator of exosome biogenesis and is responsible for age-dependent changes in exosome quantity and quality.
    DOI:  https://doi.org/10.1038/s41556-024-01481-0
  8. Heliyon. 2024 Aug 15. 10(15): e35219
      Diabetic cardiomyopathy (DCM) is a common complication of diabetes, and its pathogenesis remains elusive. Ferroptosis, a process dependent on iron-mediated cell death, plays a crucial role in DCM via disrupted iron metabolism, lipid peroxidation, and weakened antioxidant defenses. Hyperglycemia, oxidative stress, and inflammation may exacerbate ferroptosis in diabetes. This review emphasizes the interaction between cardiac fibroblasts and cardiomyocytes in DCM, influencing ferroptosis occurrence. By exploring ferroptosis modulation for potential therapeutic targets, this article offers a fresh perspective on DCM treatment. The study systematically covers the interplay, mechanisms, and targeted drugs linked to ferroptosis in DCM development.
    Keywords:  Cardiac fibroblasts; Cardiomyocytes; Diabetic cardiomyopathy; Ferroptosis; Therapeutic targets
    DOI:  https://doi.org/10.1016/j.heliyon.2024.e35219
  9. J Mol Cell Cardiol. 2024 Aug 21. pii: S0022-2828(24)00135-4. [Epub ahead of print]195 103-109
      It is still debated whether changes in metabolic flux are cause or consequence of contractile dysfunction in non-ischemic heart disease. We have previously proposed a model of cardiac metabolism grounded in a series of six moiety-conserved, interconnected cycles. In view of a recent interest to augment oxygen availability in heart failure through iron supplementation, we integrated this intervention in terms of moiety conservation. Examining published work from both human and murine models, we argue this strategy restores a mitochondrial cycle of energy transfer by enhancing mitochondrial pyruvate carrier (MPC) expression and providing pyruvate as a substrate for carboxylation and anaplerosis. Metabolomic data from failing heart muscle reveal elevated pyruvate levels with a concomitant decrease in the levels of Krebs cycle intermediates. Additionally, MPC is downregulated in the same failing hearts, as well as under hypoxic conditions. MPC expression increases upon mechanical unloading in the failing human heart, as does contractile function. We note that MPC deficiency also alters expression of enzymes involved in pyruvate carboxylation and decarboxylation, increases intermediates of biosynthetic pathways, and eventually leads to cardiac hypertrophy and dilated cardiomyopathy. Collectively, we propose that an unbroken chain of moiety-conserved cycles facilitates energy transfer in the heart. We refer to the transport and subsequent carboxylation of pyruvate in the mitochondrial matrix as an example and a proposed target for metabolic support to reverse impaired contractile function.
    Keywords:  Cardiac metabolism; Energy transfer; Heart failure; Metabolic cycles
    DOI:  https://doi.org/10.1016/j.yjmcc.2024.08.002