Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy
Curr Mol Med. 2024 Apr 5. doi: 10.2174/0115665240287631240321072504. Online ahead of print.ABSTRACTOne of the greatest serious side effects of diabetes is diabetic nephropathy (DN), which is also the key factor in the sometimes-deadly diabetic end-stage renal disease. Progressive renal interstitial fibrosis is closely associated with oxidative stress, and the extracellular matrix is typically a feature of DN. Some RNAs formed by genome transcription that are not translated into proteins are recognized as noncoding RNAs. It has been shown that ncRNAs control apoptosis, inflammatory response, cell proliferation, autophagy, a...
Source: Current Molecular Medicine - April 9, 2024 Category: Molecular Biology Authors: Yuye Zhu Chunying Liu Jamal Hallajzadeh Source Type: research

Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy
Curr Mol Med. 2024 Apr 5. doi: 10.2174/0115665240287631240321072504. Online ahead of print.ABSTRACTOne of the greatest serious side effects of diabetes is diabetic nephropathy (DN), which is also the key factor in the sometimes-deadly diabetic end-stage renal disease. Progressive renal interstitial fibrosis is closely associated with oxidative stress, and the extracellular matrix is typically a feature of DN. Some RNAs formed by genome transcription that are not translated into proteins are recognized as noncoding RNAs. It has been shown that ncRNAs control apoptosis, inflammatory response, cell proliferation, autophagy, a...
Source: Current Molecular Medicine - April 9, 2024 Category: Molecular Biology Authors: Yuye Zhu Chunying Liu Jamal Hallajzadeh Source Type: research

Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy
Curr Mol Med. 2024 Apr 5. doi: 10.2174/0115665240287631240321072504. Online ahead of print.ABSTRACTOne of the greatest serious side effects of diabetes is diabetic nephropathy (DN), which is also the key factor in the sometimes-deadly diabetic end-stage renal disease. Progressive renal interstitial fibrosis is closely associated with oxidative stress, and the extracellular matrix is typically a feature of DN. Some RNAs formed by genome transcription that are not translated into proteins are recognized as noncoding RNAs. It has been shown that ncRNAs control apoptosis, inflammatory response, cell proliferation, autophagy, a...
Source: Current Molecular Medicine - April 9, 2024 Category: Molecular Biology Authors: Yuye Zhu Chunying Liu Jamal Hallajzadeh Source Type: research

Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy
Curr Mol Med. 2024 Apr 5. doi: 10.2174/0115665240287631240321072504. Online ahead of print.ABSTRACTOne of the greatest serious side effects of diabetes is diabetic nephropathy (DN), which is also the key factor in the sometimes-deadly diabetic end-stage renal disease. Progressive renal interstitial fibrosis is closely associated with oxidative stress, and the extracellular matrix is typically a feature of DN. Some RNAs formed by genome transcription that are not translated into proteins are recognized as noncoding RNAs. It has been shown that ncRNAs control apoptosis, inflammatory response, cell proliferation, autophagy, a...
Source: Current Molecular Medicine - April 9, 2024 Category: Molecular Biology Authors: Yuye Zhu Chunying Liu Jamal Hallajzadeh Source Type: research

Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy
Curr Mol Med. 2024 Apr 5. doi: 10.2174/0115665240287631240321072504. Online ahead of print.ABSTRACTOne of the greatest serious side effects of diabetes is diabetic nephropathy (DN), which is also the key factor in the sometimes-deadly diabetic end-stage renal disease. Progressive renal interstitial fibrosis is closely associated with oxidative stress, and the extracellular matrix is typically a feature of DN. Some RNAs formed by genome transcription that are not translated into proteins are recognized as noncoding RNAs. It has been shown that ncRNAs control apoptosis, inflammatory response, cell proliferation, autophagy, a...
Source: Current Molecular Medicine - April 9, 2024 Category: Molecular Biology Authors: Yuye Zhu Chunying Liu Jamal Hallajzadeh Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy
CONCLUSION: Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.PMID:38549521 | DOI:10.2174/0115665240272051240122074511 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 29, 2024 Category: Molecular Biology Authors: Wei Yin Jin-Hua Wang Yu-Mei Liang Kang-Han Liu Ying Chen Yusa Chen Source Type: research

CXCL13-neutralizing Antibody Alleviate Chronic Skeletal Muscle Degeneration in a Mouse Model
CONCLUSION: Our study reveals the underlying therapeutic implications of CXCL13 inhibition for clinical intervention in skeletal muscle degeneration, thereby improving patient prognosis.PMID:38500285 | DOI:10.2174/0115665240275029240306045214 (Source: Current Molecular Medicine)
Source: Current Molecular Medicine - March 19, 2024 Category: Molecular Biology Authors: Zhongcheng Xie Jimin Yang Chunmeng Jiao Hui Chen Siyu Ouyang Zhiyang Liu Qin Hou Jifeng Liu Source Type: research