Mitochondrial permeability transition and its regulatory components are implicated in apoptosis of primary cultures of rat proximal tubular cells exposed to lead.
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Chronic Kidney Disease and Exposure to Nephrotoxic MetalsAntagonistic effects of selenium on lead-induced autophagy by influencing mitochondrial dynamics in the spleen of chickensPARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathwayAccumulation of methylglyoxal and d-lactate in Pb-induced nephrotoxicity in rats.Caspase-Dependent and Caspase-Independent Pathways Are Involved in Cadmium-Induced Apoptosis in Primary Rat Proximal Tubular Cell Culture.Restoration of autophagy by puerarin in lead-exposed primary rat proximal tubular cells via regulating AMPK-mTOR signaling.Alleviation of Lead-Induced Apoptosis by Puerarin via Inhibiting Mitochondrial Permeability Transition Pore Opening in Primary Cultures of Rat Proximal Tubular Cells.Autophagy blockade and lysosomal membrane permeabilization contribute to lead-induced nephrotoxicity in primary rat proximal tubular cells.Subchronic arsenism-induced oxidative stress and inflammation contribute to apoptosis through mitochondrial and death receptor dependent pathways in chicken immune organs.Down-regulation of microRNA-155 promotes selenium deficiency-induced apoptosis by tumor necrosis factor receptor superfamily member 1B in the broiler spleen.Trehalose protects against cadmium-induced cytotoxicity in primary rat proximal tubular cells via inhibiting apoptosis and restoring autophagic flux.Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway.Arsenic and/or copper caused inflammatory response via activation of inducible nitric oxide synthase pathway and triggered heat shock protein responses in testis tissues of chicken.CaMKII is involved in subcellular Ca2+ redistribution-induced endoplasmic reticulum stress leading to apoptosis in primary cultures of rat proximal tubular cells exposed to lead.Alleviation of cadmium-induced oxidative stress by trehalose via inhibiting the Nrf2-Keap1 signaling pathway in primary rat proximal tubular cells.Involvement of mitochondrial pathway in environmental metal pollutant lead-induced apoptosis of chicken liver: perspectives from oxidative stress and energy metabolism.Anti-apoptotic role of spermine against lead and/or gamma irradiation-induced hepatotoxicity in male rats.Selenium Protects against Lead-induced Apoptosis via Endoplasmic Reticulum Stress in Chicken Kidneys.CDP-choline circumvents mercury-induced mitochondrial damage and renal dysfunction.Dysfunction of cortical synapse-specific mitochondria in developing rats exposed to lead and its amelioration by ascorbate supplementation.Hirsutine induces mPTP-dependent apoptosis through ROCK1/PTEN/PI3K/GSK3β pathway in human lung cancer cells.
P2860
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P2860
Mitochondrial permeability transition and its regulatory components are implicated in apoptosis of primary cultures of rat proximal tubular cells exposed to lead.
description
2015 nî lūn-bûn
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2015年の論文
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年學術文章
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2015年學術文章
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2015年學術文章
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name
Mitochondrial permeability tra ...... tubular cells exposed to lead.
@en
type
label
Mitochondrial permeability tra ...... tubular cells exposed to lead.
@en
prefLabel
Mitochondrial permeability tra ...... tubular cells exposed to lead.
@en
P2093
P2860
P1476
Mitochondrial permeability tra ...... tubular cells exposed to lead.
@en
P2093
Du-Bao Yang
Zhen-Yong Wang
Zhong-Kun Wang
Zong-Ping Liu
P2860
P2888
P304
P356
10.1007/S00204-015-1547-0
P577
2015-06-17T00:00:00Z