We are analyzing https://link.springer.com/article/10.1007/s11010-025-05297-w.

Title:
Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis | Molecular and Cellular Biochemistry
Description:
The incidence and hospitalization rate of kidney disease, especially end-stage renal disease, have increased significantly, which seriously endangers the health of patients. Mitochondria are the core organelles of cellular energy metabolism, and their dysfunction can lead to kidney energy supply insufficiency and oxidative stress damage, which has become a global public health problem. Studies have shown that the disturbance of mitochondrial quality control mechanisms, including mitochondrial dynamics, autophagy, oxidative stress regulation and biosynthesis, is closely related to the occurrence and development of renal fibrosis (RF). As a multicellular pathological process, RF involves the injury and shedding of podocytes, the transdifferentiation of renal tubular epithelial cells, the activation of fibroblasts, and the infiltration of macrophages, among which the mitochondrial dysfunction plays an important role. This review systematically elaborates the molecular mechanisms of mitochondrial damage during RF progression, aiming to provide theoretical foundations for developing novel therapeutic strategies to delay RF advancement.
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Keywords {🔍}

pubmed, article, google, scholar, cas, mitochondrial, central, kidney, renal, fibrosis, cell, disease, injury, diabetic, physiol, dysfunction, mitophagy, rev, nephrol, liu, autophagy, nat, acute, cells, wang, int, yang, tubular, chronic, biol, med, stress, activation, protects, inflammation, damage, role, oxidative, dis, zhang, metabolic, promotes, reactive, oxygen, species, huang, clin, attenuates, nature, mechanisms,

Topics {✒️}

m-csf/m-csfr signalling activating calcium-nfatc1-bmi1 axis amp-activated protein kinase month download article/chapter drp1-mediated mitochondrial fission phosphate-induced mitochondrial injury mitochondrial-targeted compound ss-31 renal ischemia-reperfusion injury intracellular nad+/nadh ratio de ranitz-greven wl ros-induced ros release tubular epithelial cells end-stage renal disease bnip3-mediated mitophagy protects albumin-induced cell damage anti-renal fibrosis drug han-yinan yang atg5-mediated autophagy deficiency pgc-1α promotes recovery jun-rong du mir-4516/siah3/pink1 axis ischemic preconditioning-conferred renoprotection renal tubular cells inhibiting gsk-3β activity endoplasmic reticulum-mitochondrial contacts pgc-1α-mediated regulation cell-specific translational profiling reactive oxygen species park2-mediated mitophagy full article pdf proximal tubules protects mesenchymal stem cells ischemia-reperfusion injury impairs renal recovery alleviates kidney injury renal mitochondrial injury monocyte-derived alveolar macrophages inhibiting mitochondrial fission unilateral ureteral obstruction mitochondrial dynamics controls fundc1-dependent mitophagy treating renal fibrosis ucp2 attenuates apoptosis chronic kidney disease chronic kidney disease protect kidney fibrosis stress-induced mitophagy pgc-1α inhibits article wu promotes lung fibrosis

Questions {❓}

Vierhout M, Ayoub A, Naiel S et al (2021) Monocyte and macrophage derived myofibroblasts: is it fate?

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