File:Proposed CL remodeling pathways in obesity and aging.png

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Summary

Description
English: Aging and obesity cause oxidative stress, leading to the production of ROS. CL oxidation by ROS triggers the remodeling of its fatty acyl chains, which begins with hydrolysis of oxidized CL by phospholipase A2 (cPLA2), followed by acylation of lysocardiolipin by either tafazzin (TAZ), MLCLAT, or ALCAT1. TAZ is a transacylase that catalyzes physiological remodeling of CL with other phospholipids, such as PC and PE, whereas MLCLAT catalyzes remodeling of CL with MLCL and linoleoyl-CoA, leading to mitochondrial recovery. ALCAT1 catalyzes remodeling of CL with both MLCL or dilysocardiolipin and docosahexaenoic-CoA (C22:6) as substrates, leading to CL peroxidation by ROS and mitochondrial dysfunction.
Date
Source Zhang, Jun; Shi, Yuguang (2022-06-12). "In Search of the Holy Grail: Toward a Unified Hypothesis on Mitochondrial Dysfunction in Age-Related Diseases". Cells. 11 (12): 1906. doi:10.3390/cells11121906. ISSN 2073-4409. PMC 9221202. PMID 35741033.
Author Zhang, Jun; Shi, Yuguang

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Captions

Proposed CL remodeling pathways in obesity and aging.

1 June 2022

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current07:13, 3 March 2023Thumbnail for version as of 07:13, 3 March 20233,403 × 2,182 (2.26 MB)KostyaRenUploaded a work by Zhang, Jun; Shi, Yuguang from Zhang, Jun; Shi, Yuguang (2022-06-12). "In Search of the Holy Grail: Toward a Unified Hypothesis on Mitochondrial Dysfunction in Age-Related Diseases". Cells. 11 (12): 1906. doi:10.3390/cells11121906. ISSN 2073-4409. PMC 9221202. PMID 35741033. with UploadWizard
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